1 Difficulties in the Management of Bile Duct

Home , Anal fistula, Biliary fistula, Hepatectomy, Omentopexy, Stapled hemorrhoidopexy

CONTENTS

Page

Welcome Note 3 Provisional programme 4-6

MANAGEMENT OF COAGULOPATHY AFTER TRAUMA OR MAJOR SURGERY Thabo g. Mothabeng 1 military hospital 7-15

CHALLENGES IN MANAGEMENT OF INHALATION INJURY Mr. Adelin Muganza, MD, FRCSI, FCS (SA), Director Johnson and Johnson Burn Centre Chris Hani Baragwanath Academic Hospital, University of Witwatersrand, Johannesburg 16-22

PERFORATED DUODENAL ULCER LEAK POST REPAIR: A REVIEW B Singh, S Mewa Kinoo, Department of Surgery, University of KwaZulu-Natal and King Edward VIII Hospital Durban 23-27

APPROACH TO MANAGEMENT OF ANASTOMOTIC BREAK DOWN AFTER OESOPHAGECTOMY Taole Mokoena D Phil FRCS 28-32

MANAGEMENT OF THE OPEN ABDOMEN (LAPAROSTOME) USING TEMPORARY ABDOMINAL CLOSURE (TAC) Prof Jan P Pretorius 33-40

MANAGEMENT CHALLENGES PRESENTED BY ENTEROCUTANEOUS AND ENTEROATMOSPHERIC FISTULA IN CURRENT PRACTICE B Singh, S Mewa Kinoo, R Naidoo, Department of Surgery, University of KwaZulu-Natal and King Edward VIII Hospital, Durban 41-45

RECTOVAGINAL FISTULA (RVF) Dr BH Pienaar 46-50

DIFFICULTIES IN THE MANAGEMENT OF BILE DUCT INJURIES AFTER LAPAROSCOPIC CHOLECYSTECTOMY MD Smith 51-53

POST-HEPATECTOMY LIVER FAILURE Dr C Jeske, Department of Surgery, University of Pretoria and Steve Biko Acadmic Hospital 54-66

CHALLENGES IN THE MANAGEMENT OF GASTROSCHISIS AND EXOMPHALOS Dr E Müller 67-70

MALDESCENDED TESTIS IN ADULTS Dr. Evelyn M Moshokoa, HOD Urology 71-76 COMPLICATIONS AND SEQUELAE OF INGUINAL HERNIA REPAIR Prof Zach Koto, Department of Surgery, Sefako Makgatho Health Sciences University 77-79

SURGICAL CONTROVERSIES SYMPOSIUM 3 & 4 OCTOBER 2015 Problems of continence following surgery for haemorrhoids: surgical misadventure or unavoidable complication Dr Stephen Grobler, Bloemfontein 80-84

ANASTOMOTIC FAILURE IN COLORECTAL SURGERY: HOW CAN WE REDUCE THE RISK? Prof Paul Goldberg 85-87

COMPLICATIONS OF PERIANAL ABSCESSES AND THOSE OF THEIR MANAGEMENT Prof OD Montwedi 88-92

COMPLICATIONS OF ACUTE APPENDICITIS AND OF THEIR TREATMENT Dr Brandon Jackson, Department of Surgery, Faculty of Health Sciences, University of Pretoria 93-99

COMPLICATIONS OF TOTAL THYROIDECTOMY Prof LM Ntlhe 100-108

SERIOUS COMPLICATIONS AFTER COMMON SURGICAL PROCEDURES: PREVENTION AND MANAGEMENT OF THYROID CRISIS Luvhengo TE, Department of Surgery, Charlotte Maxeke Johannesburg Academic Hospital and University of the Witwatersrand 109-112

MANAGEMENT OF COMPLICATIONS OF PAROTIDECTOMY Dr J K Jekel – Dept surgery University of Pretoria 113-116

FAILURE OF BREAST RECONSTRUCTION AFTER BREAST CANCER SURGERY Dr S. Sehlale, Department Plastic Surgery 117-118

COMPLICATIONS OF CAROTID STENOSIS SURGERY T.V. Mulaudzi, Vascular Surgeon 119-123

ARE SURGEONS VIGILANT ENOUGH FOR THROMBO-EMBOLIC DISEASE? Y-N S.C Tsotetsi: Vascular Surgeon 124-126

IS THE PUBLIC HEALTHCARE SYSTEM DOING ENOUGH TO PREVENT AND MANAGE THROMBOEMBOLIC DISEASE UNDER A HEALTHCARE RESOURCE CONSTRAINT ENVIRONMENTZ? CAN THE HEALTHCARE PRACTITIONER BE ABSOLVED? Professor David McQuoid-Mason, Centre for Socio-legal Studies, University of KwaZulu-Natal, Durban 127-129

Welcome Note 2015

Once again welcome to the 2015 19th Annual Controversies and Problems in Surgery Symposium.

I should thank those patrons who participate year in year out for your loyalty, and welcome especially our novices who are attending for the first time.

I need to explain the move away from a Friday to a Sunday. The sole reason is economic. In our endeavour to keep the symposium affordable we had to book a venue within the University of Pretoria precinct, having tried other possible venues including the CSIR which turned out to be much more expensive. However the University venue was not available on the Friday, it being used for lectures. The only possible solution which we adopted was to move the programme to include the Sunday instead of the Friday. This may inconvenience some of you for which we apologize profusely.

The theme of this year is “Complications of common surgical procedures and their management”. We hope this will arm you in your practices to effectively manage such complications. The adage in the medicine that, “ if you have not had a complication from whatever procedure, it means you have not done enough”, is true. All of us will experience a complication at some stage in our careers, even from a commonly performed procedure. We should therefore arm ourselves with adequate knowledge of how to approach the management of such complications. It is the object of this year’s symposium to arm you with upto date management approach to possible complications.

I should again thank the presenters for their preparation and timeous submission of their monograms for inclusion in the proceedings. I know this takes time and effort. Please continue your contribution to this important continued professional development exercise.

One needs to once again thank the Trade for their continued support of this aspect of continuing professional development. We specifically welcome and thank new sponsors and implore them to joint the coterie of our loyal supporters and sponsors. We recognise that the economy in our country is struggling as a reflection of a worldwide economic downturn. Your support is therefore even more appreciated.

Lastly I should like to thank the members of my staff for their stellar performance as usual preparing for the symposium.

Enjoy.

Prof Taole Mokoena October 2015

PROVISIONAL PROGRAMME 19TH ANNUAL CONTROVERSIES AND PROBLEMS IN SURGERY 3RD AND 4TH OCTOBER 2015

Venue: New Lecture Theatre HW Snyman North – Faculty of Health Sciences Date: 03-04 October 2015 Theme: Complications following common operations or procedures

Date: Saturday 03 October 2015 07h15:08h00 Registration 08h00-08h05 Introduction and Welcome Prof Taole Mokoena 08h05-08h15 Opening address by the Dean Prof Eric Buch Chairman:Dr Sooraj Motilall 08h15-08h35 Management of retained clot after Dr Aldrich Jacobs ICD for haemothorax 08h35-08h55 Prevention and management of Prof Sam Mokgokong post-traumatic hypoxic brain damage 08h55-09h15 Management of coagulopathy after Dr Jeff Mothabeng trauma or major surgery 09h15-09h35 Changes of management of Dr Adeline Muganza inhalation burns 09h35-10h00 Panel discussion All participants 10h00-10h30 Tea and visit to Exhibitors Chairman: Prof Jose Ramos 10h30-10h50 Management of failed Omentopexy Prof Bugsy Singh – radical surgical or conservative approach 10h50-11h10 Management of Laparostome Prof Jan Pretorius 11h10-11h30 Complications after gastro- Prof Hein v/d Walt oesophageal reflux disease (GORD) surgery – a surgeons burden or avoidable mishaps 11h30-11h45 Approach to management of Prof Taole Mokoena anastomotic breakdown after oesophagectomy 11h45-12h00 Panel discussion All participants 12h00-13h00 Lunch and visit to Exhibitors Chairman: Dr Ramsey Maluleke/ Dr Johan v Beljon 13h00-13h20 Management of GI fistulae early Prof Bugsy Singh radical surgery or aggressive nutritional approach 13h20-13h40 Management of Pancreatic fistula Prof Jose Ramos 13h40-14h10 Management of biliary fistula Dr Thomas Marumo 14h10-14h30 Management of rectovaginal fistula Dr Hennie Pienaar 14h30-14h50 Difficulties in management of bile Prof Martin Smith duct injuries after laparoscopic cholecystectomy 14h50-15h10 Liver failure following hepatectomy Dr Christian Jeske 15h10-15h30 Panel discussion All participants 15h30-16h00 Tea and visit to Exhibitors 4

Chairman: Prof Meshack Ntlhe 16h00-16h20 Challenges in the Management of Dr Ernest Müller Gastroschisis and exompholos Issues about management of maldescended testis 16h20-16h35 (a) In childhood Dr Martin van Niekerk 16h35-16h50 (b) In adults Dr Evelyn Moshokoa 16h50-17h10 Complications and sequelae of groin Prof Zach Koto hernia repair

17h10-17h30 Panel discussion All participants Chairman: Dr Brendon Bebington 17h30-17h45 Problems of continence following Dr Stephen Grobler surgery for haemorrhoids – reflection of surgical misadventure or unavoidable complication 17h45-18h00 Anastomotic breakdown after Prof Paul Goldberg Colorectal surgery can be avoided – Y or N Liberal use of diverting colostomy a necessity 18h00-18h10 Complications of perianal Dr Daniel Montwedi abscesses and those of their management 18h10-18h20 Complications of acute appendicitis Dr Brandon Jackson and of their treatment 18h20-18h40 Panel discussion All participants 18h40-19h00 Pre-dinner Refreshments: Host: Prof Thanyani Muluadzi 19h00 Gala Dinner Host: Prof Taole Mokoena

Date: Sunday 4th October 2015

07h30 – 08h00 Registration

Chairman: Dr Thula Ngcobo 08h00-08h20 Complications of total Prof Meshack Ntlhe thyroidectomy 08h20-08h40 Prevention and management of Prof Thifheli Luvhengo thyroid crisis 08h40-09h00 Problems in the management of Dr Reshma Maharaj abnormal peri-operative calcium levels in hypercalcaemic syndromes 09h00-09h20 Management of complications of Dr Hans Jekel parotidectomy 09h20-09h40 Misculocutaneous flap failure after Dr Solly Selahle surgery for breast cancer 09h40-10h00 Panel discussion All participants 10h00-10h30 Tea and visit Exhibition Chairman: Dr B Sikhosana 10h30-10h40 Complications of carotid stenosis Prof Thanyani Mulaudzi surgery 10h40-11h00 Are surgeons vigilant enough for Dr Piet Wessels venous thrombo-embolic disease. Dr Chris Tsotetsi Y – N 11h00-11h20 Panel discussion All participants Ethics Session Chairman: Dr Elbashir Osman 11h20-11h40 Is the (public) health care system Dr Piet Wessels doing enough to prevent and Prof DJ Mcquoid-Mason management venous thromboembolic disease under health care resource constraints environment – can the health care practitioner be absolved 11h40-12h20 Panel discussion All participants 12h20-12h30 Vote of Thanks Prof Taole Mokoena

MANAGEMENT OF COAGULOPATHY AFTER TRAUMA OR MAJOR SURGERY Thabo G. Mothabeng 1 Military hospital

Trauma remains a leading cause of death among people under the age of 44 (Simmons 2014, Hess 2008, Thorsen 2011). Haemorrhage, especial from pelvic and abdominal trauma is a major contributing factor to trauma related deaths in the first 48hrs of injury. Trauma and major surgery is often complicated by a coagulopathy that makes management of the patient a formidable challenge.

The paper discusses mechanism, identification and suggested management of this acute coagulopathy. It is my aim to provoke a thought about the role of coagulation system in that bleeding patient during abdominoperineal surgery; following a ‘cholecystectomy gone wrong’ or ‘the severely injured, hypotensive patient with an open abdomen, a pH of 7.0, oozing everywhere, whose bleeding will not stop nor blood made to clot’.

Definition Acute coagulopathy complicating trauma or major surgery has been described over a decade ago and is gaining greater recognition as a clinical problem. It has been identified as a unique derangement that is distinct from disseminated coagulopathy (DIC) as commonly seen in sepsis or other conditions (Levi, 2007). Recognizing that applying generic terminology of “DIC” to this phenomenon is unhelpful and potentially counterproductive, various studies have suggested alternative names such as “Trauma- induced Coagulopathy” (TIC) (Spivey, 2005), “Early Coagulopathy of Trauma” (MacLeod, 2003), “Acute Traumatic Coagulopathy” (Brohi, 2003) and “Acute Coagulopathy of Trauma Shock” (ACoTS) (Hess, 2008). These names will be used in this presentation.

Significance Acute Coagulopathy of Trauma Shock complicates management of major trauma or surgery and is usually associated with hypoperfusion; it is present in a third to 25% of trauma patients on admission to the emergency unit and is associated with four fold increase in mortality (Brohi 2003, MacLeod 2003, Maegele 2007, Frith 2012)). ACoTS is an independent predictor of massive transfusion, preventable death, and increased hospital length of stay and development of multiple organ dysfunction (Cannon 1918, Maegele 2007, Brohi 2007)

Why the fuss? This is just DIC Some scholars suggest that seeking to distinguish between ACoTS and DIC is a fuss, splitting hairs and is only of academic interest. This is perhaps true, ACoTS is marked by systemic or disseminated coagulopathy and there are similarities with DIC; however, acute coagulopathy of trauma is not entirely an impairment of the coagulation cascade, it is characterized by increased fibrinolysis and systemic anticoagulation; it is also exclusively found in patient with shock. Both fibrinolysis and anticoagulation are exaggerated with worsening base deficit (Hess 2008, Cohen 2013). Understanding of this underlying pathophysiological differences is pivotal to the management this derangement.

Myth or reality Brohi and colleagues (2003) found clinically significant coagulopathy in 25% of the 1088 patients admitted to emergency department; coagulopathy developed long before administration of large volumes of fluids.

The existence of early coagulopathy has been verified in various other studies involving more than 20 thousand patients (Table 1)

Number Percentage ISS Mortality Mortality No coagulopathy Coagulopathy Brohi, 2003 1088 24 20 11 46 MacLeod, 2003 10790 28 9 6 19 Maegele, 2007 8724 34 24 8 28 Brohi, 2007 208 10 17 8 62 Rugeri, 2007 88 28 22 n/a n/a Table 1 Summary of studies of acute coagulopathy of trauma. ISS Injury Severity Score

Pathophysiology of ACoTS Classically in DIC, there is impairment of the coagulation cascade; contrary to that simple explanation, the causes of acute coagulopathy of major trauma are multifactorial. Various endogenous, biological processes as well as iatrogenic and environmental factors are important in the initiation and progress of ACoTS.

There is greater appreciation and respect for endothelium as an important driver of the main systems responsible for ACoTS (fibrinolysis and anticoagulation). The endothelium, activated by tissue factor (in the setting of hypoperfusion), produce high levels of thrombomodulin. Thrombomodulin forms a complex with thrombin reducing formation of fibrin. The thrombin-thrombomodulin complex converts protein C into activated protein C (APC), an anticoagulant serine protease enzyme, which may have a central role in the acute coagulopathy of trauma. APC modulates clotting in multiple ways, including increasing levels of plasmin and promoting fibrinolysis (Brohi 2007, Lier 2004).

APC also impairs the clotting cascade by inhibiting activated clotting factors V and VIII. Further, it has anti-inflammatory and antiapoptotic properties that may reduce secondary insults after localized tissue damage (Mosnier 2004). Unfortunately, the anticoagulant aspects of APC outweigh its protective properties after massive tissue damage.

Pathological thrombosis accompanies the coagulopathy of injury when tissue factor, a procoagulant subendothelial protein, is exposed in injured organs, particularly in cases of traumatic brain injury.

VIIa IXa Platelets Thrombin Fibrin FDP’s Xa VIII V

Plasmin

PAI-1 APC tPA

Thrombin - TM

APC TM TM TM Endothélium

FDP’S: fibrin degradation products, PAI-1: plasminogen activator inhibitor, PC: protein C, APC: activated protein C, tPA: tissue plasminogen activator, TM: thrombomodulin, ACoTS: acute coagulopathy of trauma shock

Making a diagnosis and monitoring ACoTS Anticipation, early diagnosis and monitoring of coagulopathy is vital to improved outcome; when clinical signs appear, it is late in the process and exceptional efforts must be taken to regain control. Traditional tests like prothrombin time (PT), partial thromboplastin time (PTT), platelets, and internationalized normalised ratio (INR) have been used in many studies and clinical practice to diagnose, monitor and manage coagulopathy of trauma; the predictive value of these tests are controversial and debatable (Simmons 2014, Schochl 2012).

An ideal test that is rapid, cheap, user friendly, reproducible and reliable does not exist. It is possible that viscoelastic haemostatic tests such as thromboelastography (TEG) and rotational thromboelastometry (ROTEM) come close.

These tests provide information on the time course of clot formation in whole blood and offer advantages over the conventional tests for evaluation of coagulation status in patients with massive bleeding. They offer rapid results, increased sensitivity in detecting abnormalities of haemostatic function, and perhaps the most important advantage is the ability to detect fibrinolysis (Johansson 2009).

Management of coagulopathy of trauma In the traditional approach to trauma patient resuscitation, the goal was to achieve and maintain a certain arbitrary blood pressure, urine output and to reverse metabolic acidosis. This entailed huge amount of crystalloids, colloids and blind administration of blood and blood products. This approach, sensible and noble as it may be failed to address coagulopathy and the outcome has been poor with early deaths, prolonged intensive care stay, lung injury, ARDS and septic complications.

One major progress in trauma care was the introduction of damage control surgery (DCS), an abbreviated laparotomy whose sole purpose is to control haemorrhage and contamination while 9

delaying definitive surgery for later when the patient is stable. Damage control resuscitation (DCS) on the other hand, is the analogous term for treating haemorrhagic shock by correcting coagulopathy, acidosis, and hypothermia as efficiently as possible, with concurrent efforts to control the bleeding source and avoid iatrogenic injury (Beekly 2008). The following is a brief discussion of the key steps in the management of ACoTS: Permissive hypotension Aggressive fluid resuscitation is indicated in injured patients to ensure tissue perfusion (Davis 1996, Moore 2006). It has however been demonstrated in several studies that prehospital administration of less than 1.5 litres is associated with greater chance of survival whereas larger amounts of fluids increases the incidence of ACoTS up to 40% (MacLeod 2003, Sihler 2009, Madigan 2008) and abdominal compartment syndrome (Madigan 2008). With permissive hypotension a mean blood pressure of 65mmHg or systolic pressure of 90mmHg is targeted until surgical intervention to stop haemorrhage is achieved. It is contraindicated in traumatic brain injury, coronary disease and hypertension (Berry 2012) and should limited to 120 minutes.

Blood and blood products Administration of blood in trauma resuscitation cannot be avoided; and there is overwhelming evidence of harm and mortality with use of blood and its products like fresh frozen plasma (FFP) and platelets, notwithstanding morbidity, increased length of stay, multiorgan failure, infections, transfusion overload, transfusion related lung injury (TRALI) and sepsis (Lelubre 2009).

The focus has shifted to questions such as the right trigger haemoglobin, the ratios of fresh frozen plasma (FFP) to packed red blood cells (PRBC). Literature seems to suggest that higher ratios of FFP to PRBC favour reduced mortality (Mitra 2012, Holcomb 2007, Maegele 2007). There are however no randomised controlled trials to proof this.

More than the debates about the right ratio of plasma to blood, the focus should be on identifying patients who will require massive transfusion. Massive transfusion is actually an important determinant of outcome and implementation of massive transfusion protocols (MTP) has been shown to improve outcome with decrease in early deaths due to bleeding (Dente 2009, Griffee 2010)

Clinical criteria to identify patients who will benefit from massive transfusion protocol lack ability to adequately pick these patients; several scores have been devised with varied predictive value. The Trauma Associated Severe Haemorrhage (TASH) score and Shock Index (SI) seem to offer high predictive value for massive transfusion (Brogman 2011, Mutschler 2013). Finally, although the recommended ratio of plasma, blood and platelets is 1:1:1, massive transfusion protocol gives a logical sequential approach to blood transfusion and blood product replacement.

Rewarming Hypothermia, defined as core body temperature lower than 35 degrees C, has an incidence of 1.6 to 8.2 percent in trauma victims (Holcomb 2007). It is not clear if the low temperatures in patients with poor outcome are a marker of severity of injury and physiologic derangement or cause of mortality; however, patients with core temperatures of less than 32 have high mortality (Shafi 2013). Early attempts should be made to limit heat loss; use of warmed fluids and both passive ℃ 10

and active warming should be employed.

Correction of acidosis Serum lactate and base deficits measurements give good idea of the severity of shock and hypoperfusion. In clinical practice, serial values of lactate are useful in predicting survival and have been used to assess response to therapy. Similarly, base deficit can independently predict mortality and is especially useful in inebriated patients likely to have falsely elevated lactate levels (Cherian 2014). Restoration of normal perfusion aimed at correcting base deficit and pH is the mainstay of treating and preventing acidosis. It may be necessary to restore volume with blood and blood products to manage acidosis and avoid giving excessive amounts of fluids crystalloids or colloids).

Pharmacological methods of controlling bleeding Antifibrinolytics Tranexamic acid (TxA) was studied in a double blinded, randomised, multicentre trial (clinical randomisation of an antifibrinolytic in significant haemorrhage, CRASH 2) involving over ten thousand adult trauma patients, and shown to significantly reduce “all cause” mortality and mortality due to bleeding (Roberts 2011). Greatest benefit is when administered within 3 hours of trauma, in a dose of 1-2g over 10min and repeat 1g over 8 hours (Lier 2011, Spahn 2013)

Recombinant factor Ⅶ Very high dose of recombinant factor Ⅶa (rFⅦa) are required for the formation of tissue factor complex to activate the clotting system. rFVIIa bypasses several steps of coagulation and interacts directly with activated platelets to form thrombin. Early use of rFⅦa was associated with a decreased 24 hour and 30 day mortality in severely injured combat patients (Spinella 2008, Boffard 2005). It has also been shown to decrease transfusion requirements in blunt trauma patients (Duchesne 2008, Berkhof 2009). Recombinant FVIIa is used as an off label agent in many massive transfusion protocols, and the reported rate of thromboembolism is small.

Combination of fibrinogen and prothrombin complex concentrates Use of prothrombin complex concentrates (PCC) can reduce the risk of transfusion associated acute lung injury and other viral infections. In a study on combat related trauma requiring massive transfusion, high fibrinogen to RBC ratio (> 1 g/L to 5 units packed RBCs) was found to decrease death from haemorrhage. A fibrinogen level of > 1.5 g/L should be maintained following trauma (Lier 2008) and transfusion of fibrinogen or cryoprecipitate may be considered if it is below this level. PCC or a complex of factors Ⅱ, Ⅶ, Ⅸ, Ⅹis found to shorten the time to coagulation and reduce blood loss following trauma (Lier 2011).

Rapid control of bleeding Haemostatic resuscitation and damage control surgery are vital components in the management and prevention of ACoTS and these strategies are best employed early before patients are at the end of their physiological reserves.

CONCLUSION The last five years have seen tremendous advances in our understanding of acute coagulopathy of trauma. Although studies determining the influences of single preconditions to traumatic coagulopathy are interesting for scientific purposes, in the clinical setting, ACoTS and the deterioration of haemostasis in trauma is always caused by multiple and concurring ones.

We maybe far from having all the answers, but we understand that coagulopathy sets in much earlier than traditionally believed. Trauma shock and tissue hypoperfusion are central to the causati on of early ACoTS. Routine tests of coagulation are inadequate in diagnosing or monitoring coagulopathy and should be replaced by better tests. Presently viscoelastic hemostatic assays are the most reliable among existing tests in monitoring coagulopathy. Damage control resuscitation is the umbrella term to several measures, including but not limited to permissive hypotension, blood, platelets and plasma transfusions, recombinant factors, that can counter worsening of coagulopathy and result in a reduction of morbidity and mortality.

References and suggested reading 1. Beekley AC. Damage control resuscitation: a sensible approach to the exsanguinating surgical patient. Crit Care Med 2008; 36 (Suppl):S267–S274. 2. Berkhof FF, Aikenboom JCJ. Efficacy of recombinant activated factor Vii in patients with massive uncontrolled bleeding: A retrospective observational analysis. Transfusion 2009 ; 62:1095 – 1099 3. Berry C, Ley EJ, Bukur M, Malinoski D, Margulies DR, Mirocha J, Salim A. Redefining hypotension in traumatic brain injury. Injury 2012; 43: 1833-1837 4. Boffard KD, Riou B, Warren B, et al. Recombinant factor VIIa as adjunctive therapy for bleeding control in severely injured trauma patients: two parallel randomized, placebo- controlled, double-blind clinical trials. J Trauma 2005; 59:8–15. 5. Borgman MA, Spinella PC, Holcomb JB, Blackbourne LU, Wade CE, Lefering R, Bouillon B, Meagele M. The effect of FFP to RBC ratio on morbidity and mortality in trauma patients based on transfusion prediction score. Vox sanguinis 2011 ; 101 (1) 44 – 54 6. Brohi K, Singh J, Heron M, et al. Acute traumatic coagulopathy. J Trauma 2003; 54:1127–1130. 7. Brohi K, Cohen MJ, Ganter MT, et al. Acute traumatic coagulopathy: initiated by hypoperfusion: modulated through the protein C pathway? Ann Surg 2007; 245:812–818 8. Brohi K, Mitchell J. Cohen and Ross A. Davenport. Acute coagulopathy of trauma: mechanism, identification and effect. Current Opinion in Critical Care 2007, 13:680–685 9. Cannon W, Frawer J, Cowell E. The preventive treatment of wound shock. JAMA 1918; 70:618–621. 10. Davis JW, Parks SN, Kaups KL, Gladen HE, O’Donnell-Nicol S. Admission base deficit predicts transfusion requirements and risk of complications. J Trauma 1996; 41: 769-774 11. Duchesne JC, Matthew AA, Marr AB et al. Current evidence based guidelines for factor VIIa use in trauma: The good, the bad, and the ugly. Am Surg 2008; 12

74:1159 – 1165 12. Frith Acute traumatic coagulopathy. Current Opin Anaesthesiol 2012, 25:229-234 13. Griffee MJ, DeLoughery TG, Thorborg PA. Coagulation management in massive bleeding. Current Opinion in Anaeshesiol 2010: 23: 000 – 000 14. Hess JR, MD, MPH, FACP, FAAAS, Karim Brohi, MD, Richard P. Dutton, MD, MBA, Carl J. Hauser, MD, FACS, FCCM, John B. Holcomb, MD, FACS, Yoram Kluger, MD, Kevin Mackway-Jones, MD, FRCP, FRCS, FCEM, Michael J. Parr, MB, BS, FRCP, FRCA, FANZCA, FJFICM. The Coagulopathy of Trauma: A Review of Mechanisms. J Trauma. 2008; 65:748 –754. 15. Holcomb JB, Jenkins D, Rhee P, et al. Damage control resuscitation: directly addressing the early coagulopathy of trauma. J Trauma 2007; 62:307–310. 16. Johansson PI, Stissing T, Bochsen L, Ostrowski SR. Thrombelastography and thromboelastometry in assessing coagulopathy of trauma. Scand J Trauma Resusc Emerg Med 2009; 17:45. 17. Ketchum L, MD, John R. Hess, MD, MPH and Seppo Hiippala, MD. Indications for Early Fresh Frozen Plasma, Cryoprecipitate, and Platelet Transfusion in Trauma. J Trauma. 2006; 60:S51–S58. 18. Lelubre C, Piagnerelli M, Vincent JL. Association between duration of storage of transfused red blood cells and morbidity and mortality in adult patients: myth or reality? Transfusion 2009; 49:1384–1394. 19. Lier H, Krep H, Schoechl H. Coagulation management in the treatment of multiple trauma. Anesthetist 2009; 58:1010–1026. 20. Lier H, Böttiger BW, Hinkelbein J, Krep H, Bernhard M. Coagulation management in multiple trauma: a systematic review. Intensive Care Med 2011; 37: 572-582 21. Macleod JBA, Lynn M, McKenney MG, et al. Early coagulopathy predicts mortality in trauma. J Trauma 2003; 55:39–44. 22. Madigan MC, Kemp CD, Johnson JC, Cotton BA. Secondary abdominal compartment syndrome after severe extremity injury: are early, aggressive fluid resuscitation strategies to blame? J Trauma 2008; 64: 280-285 23. Maegele M, Lefering R, Yucel N, et al. Early coagulopathy in multiple injury: an analysis from the German Trauma Registry on 8724 patients. Injury 2007; 38:298–304. 24. Mitra B, Cameron PA, Mori A, Fitzgerald M. Acute coagulopathy and early deaths post major trauma. Injury 2012; 43:22–25. 25. Moore FA, McKinley BA, Moore EE, Nathens AB, West M, Shapiro MB, Bankey P, Freeman B, Harbrecht BG, Johnson JL, Minei JP, Maier RV. Inflammation and the Host Response to 26. Injury, a large-scale collaborative project: patient-oriented research core-- standard operating procedures for clinical care. III. Guidelines for shock resuscitation. J Trauma 2006; 61: 82-89 27. Mosnier LO, Gale AJ, Yegneswaran S, Griffin JH. Activated protein C variants with normal cytoprotective but reduced anticoagulant activity. Blood 2004; 104:1740–1744. 28. Rizoli SB, MD, PhD, FRCSC, Tetsuo Yukioka, MD, David B. Hoyt, MD, FACS, and Bertil Bouillon, MD 29. Sihler KC, Napolitano LM. Massive transfusion: new insights. Chest 2009; 136: 1654-1667

30. Shafi S, Elliott AC, Gentilello L. Is hypothermia simply a marker of shock and injury or an independent risk factor for mortality in trauma patients? Analysis of a large trauma registry. J Trauma 2005, 59:1081

31. Spahn DR, Bouillon B, Cerny V, Coats TJ, Duranteau J, Fernández-Mondéjar E, Filipescu D, Hunt BJ, Komadina R, Nardi G, Neugebauer E, Ozier Y, Riddez L, Schultz A, Vincent JL, Rossaint R. Management of bleeding and coagulopathy following major trauma: an updated European guideline. Crit Care 2013; 17: R76 32. Spinella PC, Perkins JG, McLaughlin DF, Niles SE, Grathwohl KW, Beekley AC, Salinas J, Mehta S, Wade CE, Holcomb JB. The effect of recombinant activated factor VII on mortality in combat-related casualties with severe trauma and massive transfusion. J Trauma 2008; 64: 286- 293.

Invited Commentary: Dr S Motilal, Head of Trauma, UP

Protocol for Management of Massive Transfusion

Sequence of Components

Profound hypotension should be treated speedily. Administer crystalloid or colloid infusions rather than delay fluid administration. Initial red cell replacement is in the form of packed red cells.

Laboratory Samples

At the start of resuscitation, blood should be taken for group and crossmatch, coagulation tests, full blood count and biochemistry. These must be properly labelled and identified in all situations.

Blood Bank Arrangements

Routine procedures should be followed until it becomes obvious that massive transfusion is likely. The blood bank should be informed as soon as possible that a major trauma is arriving or in the building.

For extreme emergencies group O blood should be supplied first. Rhesus D negative blood should be supplied to all women of childbearing age. Type specific (ABO Rh D matched) blood should be available in 5 minutes and the switch should be made promptly so as not to deplete stores of group O blood. Continue transfusing blood on this basis until time is available to crossmatch on the original serum sample. If an antibody screen is negative and more than one blood volume has been administered there is no point attempting compatibility tests except to exclude ABO mismatches.

Monitoring During massive transfusion, regular monitoring of haemoglobin, platelet count, prothrombin time (PT), partial thromboplastin time (PTT) and fibrinogen levels should take place and be used to guide component replacement.

Components Component replacement should occur only in the presence of active bleeding or if interventional procedures are to be undertaken.

Platelet concentrates (1 pack/10kg) are given if platelet count falls below 50. Each platelet concentrate also provides around 50ml of fresh plasma. Fresh frozen plasma (12ml/kg)is administered if PT or PTT are running higher than 1.5 times control levels. Cryoprecipitate (1-1.5 packs/10kg) is given for Fibrinogen levels < 0.8g/l.

For massive uncontrolled traumative haemorrhage, maintenance of full hemostatic ability is usually unrealistic. The priority is for definitive surgical arrest of haemorrhage from major vessels. Combinations of stored whole blood, packed cells, colloids & crystalloids are given to maintain blood volume or pressure at adequate levels and haemoglobin at around 7g/dl or haematocrit at 0.25. Conserve limited supplies of fresh blood, plasma or platelets until the bleeding is controlled. When blood loss has lessened (0.5l/hour) and major vessels have been controlled, it becomes worthwhile correcting haemostasis.

Further Reading

1. M.D. Donaldson, M.J.Seaman, G.R. Park, Massive Blood Transfusion, British Journal of Anaesthesia 1992;69:621-630 2. Blood Transfusion Task Force - Transfusion for Massive Blood Loss Clinical & Laboratory Haematology, 1988;10:265-273

Background

Many victims of fire accident have both inhalation and thermal injury. The combination of bronchopulmonary injury with cutaneous burns that exceed 40 % of the total body surface area (TBSA) causes mortality to increase more than 70 % in South Africa. Smoke inhalation may produce injury through different mechanisms. Heated air may induce significant thermal injury to upper airway. Particulate matters produced during combustion can obstruct and irritate the airways, causing bronchoconstriction. Numerous gases released from burning materials like carbon monoxide (CO), Hydrogen cyanide have toxic effect to many cells. More other lethal gases are used in military warfare with significant mortality related.

Three primary mechanisms that lead to injury in smoke inhalation:

- Thermal damage It is usually limited to oropharyngeal area. The laryngeal reflexes help to protect the lower airway from heat. Steam and aspiration of hot liquids provide some exception can affect the lower airway as moist air has much greater heat-carrying capacity than dry air.

- Pulmonary injury Inhalation of toxic products triggers a cascade of effects in the lower airway by activation of body’ inflammatory response, direct tissue injury, mucus oversecretion, acute bronchospasm and obstruction of small airways. Damage to the alveolar capillary membrane increase permeability and intravascular leakage into the pulmonary interstitium. Loss of compliance, further atelectasis, increase edema can result in severe ventilation-perfusion mismatch and hypoxia

- Asphyxiation

Tissue hypoxia can occur via several mechanisms. Combustion in a closed space can consume significant amounts of oxygen, decreasing the ambient concentration of oxygen to as low as 10-13%. For victims in that setting, the decrease in fraction of inspired oxygen (FIO2) leads to hypoxia, even if they have adequate circulation and oxygen-carrying capacity. If sufficiently severe, hypoxia can lead to multiorgan dysfunction, which substantially raises morbidity and mortality. Carbon monoxide CO causes tissue hypoxia by decreasing the oxygen-carrying capacity of the blood. Hemoglobin binds CO with an affinity more than 200 times greater than the affinity for oxygen. Other mechanisms contribute, as well. CO causes a left shift in the oxyhemoglobin saturation dissociation curve, which reduces the ability of hemoglobin to unload oxygen.

The heart is particularly affected because CO binds with the heme molecules in myoglobin, decreasing facilitated diffusion of oxygen into muscle. Interaction of CO with myocardial myoglobin results in decreased myocardial contractility. The literature suggests that hypoxic encephalopathy secondary to CO poisoning results from a reperfusion injury in which the products of lipid peroxidation and free radical formation contribute to morbidity and mortality. Cyanide Cyanide (CN) gas can be produced by combustion of the following: plastics, paper products, rubber, wood and others CN directly stimulates chemoreceptors of carotid and aortic bodies, leading to a brief period of hyperpnea.] CN is a small lipophilic molecule and a chemical asphyxiant that interferes with cellular metabolism by binding to the ferric ion on cytochrome a3, subsequently halting cellular respiration. Affected cells convert to anaerobic metabolism, and lactic acidosis ensues. The organs most sensitive to cellular hypoxia are the central nervous system (CNS) and the heart. The CNS reacts to low concentrations of cyanide by promoting hyperventilation, thereby increasing exposure. Consider CN toxicity in all patients with smoke inhalation who have CNS or cardiovascular findings. Cyanide toxicity is difficult to confirm but is frequently concominant with CO toxicity. Its presence can be inferred by the presence of lactic acidosis in the right clinical setting. Even mild degrees of CN poisoning can cause delayed neurological sequelae in survivors and permanent disability including the following:

• Seizures • Various extrapyramidal syndromes • Dystonia • Postanoxic coma

Methemoglobinemia Methemoglobinemia occurs in fire due to heat denaturation of hemoglobin, oxides produced in fire, and methemoglobin-forming materials such as nitrites. Methemoglobinemia is less common in smoke inhalation injury than CN and CO toxicity. The pathophysiologic consequences of methemoglobin formation are a decrease in the oxygen-carrying capacity of the blood and a shift of the oxyhemoglobin dissociation curve to the left, similar to carboxyhemoglobin

Workup In the workup of inhalation injuries caused by toxic smoke, the primary investigation focuses on the pulmonary system. Other tests may be clinically indicated based on history, physical examination, and underlying health problems. Carbon dioxide levels also may be monitored, since patients with prior lung disease such as asthma and chronic obstructive pulmonary disease may be affected more severely and are at greater risk to retain carbon dioxide. Studies may include the following:

• Pulse oximetry and CO-oximetry • Arterial blood gases (ABGs) • Carboxyhemoglobin level 17

• Lactate • Complete blood cell count (CBC) • Chest radiography • Electrocardiogram • Serial cardiac enzymes (in patients with chest pain) • Pulmonary function testing • Direct Laryngoscopy and fiberoptic bronchoscopy

Pulse Oximetry and CO-oximetry Pulse oximetry readings can be misleading in the setting of carbon monoxide (CO) exposure or methemoglobinemia because these devices use only 2 wavelengths of light (the red and the infrared spectrum), which detect oxygenated and deoxygenated hemoglobin only and not any other form of hemoglobin. Readings are falsely elevated by CO-bound hemoglobin (carboxyhemoglobin). Arterial Blood Gases Arterial oxygen tension (partial pressure of arterial oxygen [PaO2]) does not accurately reflect the degree of CO poisoning or cellular hypoxia. The PaO2 level reflects the oxygen dissolved in blood that is not altered by the hemoglobin-bound CO. Because dissolved oxygen makes up only a small fraction of arterial oxygen content, a PaO2 level within the reference range may lead to serious underestimation of the decrement in tissue oxygen delivery and the degree of hypoxia at the cellular level that occurs when CO blocks the delivery of oxygen to the tissues. . ABG measurements are nonetheless useful to assess the adequacy of pulmonary gas exchange. Although the presence of a PaO2 level that is within the reference range may not exclude significant tissue hypoxia due to the effects of CO, the presence of a low PaO2 (< 60 mm Hg in room air) or hypercarbia (alveolar [arterial] carbon dioxide pressure [PaCO2] level of 55 mm Hg) indicate significant respiratory insufficiency. Metabolic acidosis suggests inadequate oxygen delivery to the tissues. Lactate levels associated with CN poisoning have been reported as being above 8 mmol/L.[12] The concentration of lactate increases proportionally with the amount of CN poisoning, and lactate levels higher than 10 mmol/L are a sensitive indicator of CN levels higher than 1 mg/mg.[39] Note that in most institutions, CN levels can take hours to days for results; therefore, one must rely on clinical and indirect laboratory data. Other Blood Studies Electrolyte testing can identify an anion gap acidosis. In patients who require large-volume fluid resuscitation, measure electrolytes at regular and frequent intervals to monitor for the electrolyte abnormalities that may occur in these patients. Use results to adjust both fluid and electrolyte replacement. A baseline CBC is warranted, as certain types of smoke are associated with a significant drop in hemoglobin and hematocrit beginning at 1 week postexposure. A baseline white blood cell count can also be used for comparison when concerns arise about infection Cyanide levels Cyanide levels correlate closely with the level of exposure and toxicity, but these values may not be readily available. Many hospitals send out tests for cyanide levels, and results may not return for several days to a week. In a setting consistent with potential cyanide exposure, institute specific empiric therapy while waiting for laboratory confirmation of the diagnosis. Findings indicative of cyanide intoxication include the following:

• Persistent neurologic dysfunction unresponsive to use of supplemental oxygen • Cardiac dysfunction 18

• Severe lactic acidosis, particularly in the presence of high mixed venous oxygen saturation • “Arterialization” of the venous blood gas, with PO 2 values similar to arterial levels due to lack of oxygen utilization by tissues

Radiography Obtain chest x-ray films in patients with a history of significant exposure or pulmonary symptoms. The chest film is likely to be normal—initial studies have only 8% sensitivity for smoke inhalation—but it provides a baseline for subsequent comparison in cases of significant injury. Radiographic evidence of pulmonary injury typically does not appear until 24-36 hours after the inhalation. When present, abnormal findings may include atelectasis, pulmonary edema, and acute respiratory distress syndrome (ARDS). Hyperinflation may suggest injury of the smaller airways and air trapping. In phase III of oxides of nitrogen exposure, a noncardiogenic pulmonary edema pattern may be seen on the chest radiograph. The chest radiograph may also show a pattern similar to military tuberculosis, which corresponds to a pathologic finding of classic bronchiolitis fibrosa obliterans. Fibrotic changes either may clear spontaneously or proceed to severe respiratory failure. Computed Tomography Chest computed tomography (CT) scans may show ground-glass opacities in a peribronchial distribution and/or patchy peribronchial consolidations. These findings may be present on CT scan as early as a few hours after inhalation injury. A CT scan of the brain may show signs of cerebral infarction due to hypoxia, ischemia, and hypotension. An interesting and well-reported finding for severe CO toxicity is bilateral globus pallidus low-density lesions. These lesions may not appear until several days after the exposure days. This finding is highly specific for CO insult—unlike focal cortical hypoperfusion, which is nonspecific.

Radionuclide Scintigraphy Delayed or inhomogeneous clearance of 133Xenon can be used to detect small-airway parenchymal injury. However, this study adds little to the clinical management and is not known to offer any particular therapeutic advantage. Direct Laryngoscopy and Fiberoptic Bronchoscopy A significant number of patients may present with a paucity of upper airway signs or symptoms but may still have serious subglottic injury. The threshold for performing diagnostic bronchoscopy should be low. Bronchoscopy can be diagnostic as well as therapeutic, particularly when lobar atelectasis is present. Bronchoscopy is the criterion standard for diagnosis of smoke inhalation injury. This procedure examines the airways from the oropharynx to the lobar bronchi. Although it may be performed in the ED, the intensive care unit or burn unit may be a more appropriate setting, especially in patients who are intubated. Erythema, charring, deposition of soot, edema, and/or mucosal ulceration may be present, although severe vasoconstriction from hypovolemia may mask significant injury. Impending airway obstruction may be inferred. Diagnostic accuracy is reported to be 86%. Fiberoptic bronchoscopy can also be used to facilitate endotracheal tube placement, even in the technically difficult airway.

Studies have shown up to a 96% correlation between bronchoscopic findings and the triad of closed-space smoke exposure, carboxyhemoglobin levels of 10% or greater, and carbonaceous sputum. In another study, serial bronchoscopy was twice as sensitive for diagnosing inhalation injury as clinical findings alone. Bronchoscopy is more sensitive and accurate than clinical examination alone in diagnosing inhalation injury and is, therefore, particularly useful in cases in which the decision to perform endotracheal intubation is unclear. The use of bronchoscopy in patients with inhalation injury complicated by pneumonia is associated with a decreases in the duration of mechanical ventilation, length of intensive care unit stay, and overall hospital cost.[44] Serial bronchoscopy can help remove debris and necrotic cells in cases with aggressive pulmonary toilet or when suctioning and positive pressure ventilation are insufficient. Bronchoscopy in children requires the use of a bronchoscope with a relatively small diameter, in order to accommodate the narrow pediatric airway. Extremely small diameter fiberoptic bronchoscopes with a suction port (capable of entering an endotracheal tube sized for a small toddler or infant) have only recently become available, and whether these limit the ability to remove heavy particulate matter is unclear. Emergency Department Care

Presently, no specific treatment exists to ameliorate the tissue damage and reduce the vulnerability to infection induced by smoke inhalation. Administer 100% oxygen because of the likelihood of CO inhalation in fires. Once CO toxicity, cyanide (CN) toxicity, and methemoglobinemia have been addressed, subsequent treatment is predominantly supportive. The most urgent concern in patients is the patency of the upper airway and adequacy of ventilation. Check for exposure to heat and thermal injury to the nose, mouth, face, and singed hair. Consider smoke involvement if soot is on the face and in sputum, although smoke inhalation is possible without evidence of soot. The proportion of patients with an inhalation injury who require endotracheal intubation is higher for those who also have a burn injury: 62% with a burn versus 12% without a thermal injury and the incidence of inhalation injury increases with the size of the burn. Oxidant injury eventually leads to cast formation of cellular debris in the airways, thus contributing to pulmonary failure.

Mechanical Ventilation Mechanical ventilation may be necessary in patients with inhalation injury. Use of positive pressure ventilation with low tidal volumes (3-5 mL/kg) and positive end-expiratory pressure (PEEP) and maintenance of plateau pressures below 30 cm water significantly increases short-term survival and is associated with decreased tracheobronchial cast formation. In fact, this treatment has been shown to increase the intensive care unit (ICU) survival rate. PEEP may assist in opening obstructed closed alveoli and help ventilation in those patients with poor compliance by increasing functional residual capacity. Ideally, PEEP stents alveoli open, preventing the atelectasis and alveolar flooding that can result from surfactant dysfunction, increasing interstitial fluid, and third-spacing. High-frequency percussive ventilation (HFPV), while not as commonly used in the ED, is considered standard therapy in many burn centers. HFPV generates pulsatile flow at up to 600 cycles per minute, which entrains the humidified gas by its effect on molecular diffusion. It can improve clearance of airway secretions and allow continued patency of the lower 20

airways. In patients with inhalation injury and burns involving less than 40% of total body surface area, HFPV decreases both morbidity and mortality. Not proven to improve survival compare to standard mode of ventilation with high PEEP

Pulmonary Toilet As with many respiratory conditions, the use of chest physiotherapy is widely accepted in inhalation injury. The use of percutaneous cupping and postural drainage seem reasonable to clear airways of cellular debris and soot, thereby preventing atelectasis and obstruction. Obviously, care must be taken in attempting this in the presence of significant chest wall burns. Encourage extubated patients to cough and deep breathe. In patients who are intubated, use gentle suctioning to remove mucus, debris, and sloughed epithelium. Fiberoptic bronchoscopy may be helpful in removing the debris and in facilitating pulmonary toilet. Tracheostomy The timing of tracheostomy continues to be controversial. Certainly, tracheostomy can be lifesaving for patients in whom endotracheal intubation is not possible, because of severe airway edema or burns. With early recognition of upper airway injury, this should be a rare occurrence. Tracheostomy, especially through burned tissue, has an increased complication rate and risk of sepsis when compared with endotracheal intubation. Thus, most patients can be effectively managed with endotracheal intubation through the mouth or nose. In patients expected to have a long period of convalescence because of severe neurologic or pulmonary injury, however, tracheostomy may be desirable for patient comfort and is easy to maintain.

Hyperbaric oxygen therapy (HBO) HBO therapy also displaces CO from intracellular stores and may improve mitochondrial function. HBO requires special facilities that are not available at all centers, resulting in a delay in treatment while the patient is transported to facility with HBO. Hyperbaric therapy should be considered in those patients who have high carboxyhemoglobin levels >25%, who are unconsciousness, have other neurologic findings, or have severe metabolic acidosis (ph < 7.1). The benefit of treating patients 12 hours or more after CO exposure remains unproven Epinephrine Adrenaline is used for severe bronchoconstriction, especially in patients with underlying reactive airways disease. This agent has alpha-agonist effects that include increased peripheral vascular resistance, reversed peripheral vasodilatation, systemic hypotension, and vascular permeability. The beta-agonist effects of epinephrine include bronchodilation, chronotropic cardiac activity, and positive inotropic effects. We are limited at this stage for use as adrenaline nebuliser with normo saline. Other Nebulizers Some studies have shown the use of Heparin in the form of aerosol provide a protective function and allow to clear different casts in airway. Its use is controversial. Fluid resuscitation in inhalation injury 21

It has been a topic of controversy, most of these patients have combine smoke injury and skin burns requiring fluid resuscitation. Parklane Formula is the standard guideline to provide fluid at 4ml/kg/% Burns. However some studies have suggested to give 6 ml[u1] instead of 4 ml. This approach has been criticized because of risk of overloading lungs with fluid when there is already impairment function due to smoke injury. Thus others have suggested to reduce fluid resuscitation in this case to 2-3 ml/kg/% burns. Prognosis Most inhalation injuries are self-limited and resolve within 48-72 hours. The severity of direct pulmonary parenchymal injury depends on the extent of exposure and the type of inhaled toxins produced during combustion. Most patients do not manifest spirometry changes. Rare long-term sequelae include tracheal stenosis, bronchiectasis, interstitial fibrosis, and bronchiolitis obliterans. The prognosis for mild-to-moderate exposures of toxic smokes is generally very good, with the usual outcome return to full recovery without sequelae. Metal fume fever is self-limited and usually resolves after a short period of observation. Exposure to white smoke in a military setting can lead to acute lung injury and in severe cases to ARDS. With more severe exposures, lungs may become severely damaged and develop chronic pulmonary fibrosis. Children with acute pulmonary injury from toxic inhalations generally do well once supported through the initial period of inflammation and damage. Most of the pulmonary damage is self-limited and resolves within 2-3 days. The degree of recovery depends on the extent of the pulmonary parenchymal injury and subsequent hypoxic damage to the organs.

PERFORATED DUODENAL ULCER LEAK POST REPAIR: A REVIEW B Singh, S Mewa Kinoo Department of Surgery, University of KwaZulu-Natal and King Edward VIII Hospital Durban

Perforated duodenal ulcer is one of the common surgical emergencies. The mortality following surgery for perforated duodenal ulcer (PDU) range between 6.9 – 10% globally.

Whereas the risk factors that are consistently implicated in mortality associated after surgery for PDU are well described, (table 1) an important cause of mortality (up to 56%)1 is the development of re-leak after PDU omental repair.

TABLE 1: RISK FACTORS ASSOCIATED WITH MORTALITY FOLLOWING SURGERY FOR PDU2, 3

presence of shock at admission

coexistence of significant illnesses

age > 60 years

undertaking resection surgery

time delay between perforation and operation

preoperative blood urea and serum creatinine

size of perforation

Re-leak following omentoplasty : the problem

The rate of re-leak following omentoplasty has been reported to be between 2 – 7.6%1, 4 The literature on the mechanisms that predispose to re-leaks after PDU omental repair and the therapeutic options to address this catastrophe is spare; one is reliant on guidelines based on retrospective reports.

A study by Kumar et al1 cited risk factors for re-leak following a Graham patch closure (operative techniques not detailed) (table 2)

TABLE 2: FACTORS CONTRIBUTING TO RELEAK AFTER SURGICAL CLOSURE OF PERFORATED DUODENAL ULCER BY GRAHAM'S PATCH. 1

Age > 60 years

Pulse rate > 110/minute

Blood pressure <90mmHg

Haemoglobin < 10g/dl

Serum albumin <2.5 g/dl

Total lymphocyte count < 1800 cells/mm3

Size of perforation > 5mm

Haemoglobin level, serum albumin and size of PDU were independent risk factors for prediction of re-leak on multivariate analysis. Low haemoglobin levels and serum albumin are well known factors influencing wound healing; correction of these factors (notwithstanding the urgent correction of haemoglobin level) is impractical. For this reason, the size of the PDU and the appropriate omentoplasty technique deserve consideration.

Omental patch techniques

The classic pedicled omental patch that is commonly performed for the 'plugging' of PDU was first described by Cellan-Jones in 19295 is accepted as the gold standard treatment, even though this technique has been erroneously attributed to Graham who (in 1937), described the use of a free graft of the omentum to repair PDU.6 Prior to the Cellan-Jones technique, the standard treatment was, following excision of friable edge, the application of purse string sutures covered with an omental graft. In order to obviate narrowing of the duodenum, Cellan-Jones advocated an omentoplasty without primary closure of the defect. His technique consisted of placing 4–6 sutures, selecting a pedicled omental strand with a suture through it used to anchor the omental strand in the perforation; the sutures are then tied (figure 1). In the technique described by Graham a free omental graft was used; three sutures were classically used with a piece of omentum graft laid over these sutures, which are then tied. In both techniques, no attempt is made to actually close the perforation. The technique described by Cellan-Jones was modified by Karanjia et al7; in the latter technique the omental pedicle is secured to the tip of a nasogastric tube passed through the PDU. The nasogastric tube is withdrawn for 5-6 cms before the omentum is secured to healthy serosa (figure1).

A technique described as omentopexy whereby the PPU is sutured in one layer by three interrupted sutures with a patch of pedicled omentum used to reinforce the suture line is widely used (figure 1). This technique was noted to be associated with a greater morbidity and mortality compared to omental plugging (as described by Karanjia)7. Regardless of the omentoplasty technique employed, careful securement and approximation of the sutures are important; in their report of 17 patients with re-leaks, Maghsoudi and Ghaffari 8 noted that the omental patch had gangrenous appearance in five patients and partial or complete separation of omental patch in all the patients who underwent re-laparotomy.

FIGURE 1: OPTIONS OF PERFORATED DUODENAL ULCER REPAIR

Cellan - Jones patch Graham patch Karanja plugging Omentopexy with pedicle without pedicle pulled into lumen on lay patch with pedicle with NGT

Omental patch challenges

An important decision, one of 5 (as structured by Feliciano9) facing the surgeon treating the PDU, is whether an omentoplasty is sufficient or is a definitive ulcer operation required? The former brings to light the occasional large PDU, closure of which by the simple described method may predispose to a re-leak. “Giant’ PDU are technically difficult to repair due to the complex anatomy of the duodenum, and its marginal blood supply shared with the pancreas together with extensive tissue loss and surrounding inflammation. However, there are several reports that attest to the efficacy of omentaplasty in the management of a PDU up to a diameter of 3 cms. 4, 7, 10. While Schein’s comment that “..do not stich the perforation but plug with viable omentum and patch a perforated ulcer if you can, if you cannot, then you must resect”11 has wide currency, conservative options other than omental plugging have been described; these include jejunal serosal patch, jejunal pedicled graft, proximal gastroenterology and gastric disconnection.

The recommendations for the management of re-leak following omentoplasty are based on the stability of the patient and findings at re-laparotomy. Together with reinforcement of the original omentoplasty, in the pre-proton pump era proximal gastric vagotomy without a drainage procedure was strongly recommended 12; alternate options included truncal vagotomy with antrectomy or gastreoenterostomy. More recently (in 2011), in their series of 17 patients with re-leak (from a total of 422 patients with PPD) Maghsoudi and Ghaffari 8 undertook reinsertion of omental patch and subhepatic drainage in 13 patients, subhepatic drainage in 3 patients and jejunal serosal patch in 1 patient; the overall mortality was 59%.

In the situation where reinforcement of the original omentoplasty is not feasible (friable, oedematous tissue, giant PDU, gross contamination), intubation of the PDU13 with a feeding jejunostomy or pyloric exclusion with gastroenterostomy should be considered.

Ultimately, the choice of procedure will depend on operative findings , available technical expertise and the patient’s physiological reserve. (see Figure 2)

FIGURE 2: SUGGESTED ALGORYTHM FOR LEAK OF REPAIRED PDU

PERFORATED DUODENAL ULCER

REPAIR OPTIONS

CELLEN JONES / GRAHAM / OMENTAL PLUGGING / OMENTOPLASTY

POST REPAIR LEAK

RESUSITATE PATIENT, RELOOK LAPAROTOMY / LAPAROSCOPY

STABLE PATIENT UNSTABLE PATIENT

RE-INFORCEMENT OF OMENTOPLASTY RE-INFORCEMENT OF OMENTOPLASTY + +

WIDE DRAINAGE DEFINITIVE PROCEDURE PYLORIC EXCLUSION WITHWIDE DRAINAGE FEEDING JEJUNOSTOMY GASTROENTEROSTOMYFEEDING JEJUNOSTOMY

ULCER INTUBATION CONTROL FISTULA

VAGOTOMY + GASTROENTEROSTOMY TRUNCAL VAGOTOMY + ANTRECTOMY PROXIMAL GASTRIC VAGOTOMY

References

1 Kumar K, Pai D, Srinivasan K, Jagdish S, Ananthakrishnan N. Factors contributing to releak after surgical closure of perforated duodenal ulcer by Graham's Patch. 2 Noguira C, Silva AS, Santos JN, Silva AG, Matos E, Vilaca H. Perforated peptic ulcer: main factors of morbidity and mortality. World J Surg 2003; 27(7):782-7 3 Mariëtta JOE, Bertleff A, Johan F. Lange JJ. Perforated peptic ulcer disease: a review of history and treatment. Dig Surg 2010;27:161–169 4 Gupta S,Kaushik R, Sharma R, Attri A.The management of large perforations of duodenal ulcers BMC Surgery 2005, 5:15 5 Cellan-Jones CJ. A rapid method of treatment in perforated duodenal ulcer. BMJ. 1929( 36): 1076–1077 6 Graham RR. The treatment of perforated duodenal ulcers. Surg Gynecol Obstet. 1937( 64): 235–238 7 Jani K, Saxena AK, Vaghasia R. Omental plugging for large-sized duodenal peptic perforations: A prospective randomized study of 100 patients. South Med J. 2006 May;99(5):467-71. 8 Hemmat Maghsoudi and Alireza Ghaffari. generalized peritonitis requiring re- operation after leakage of omental patch repair of perforated peptic ulcer . Saudi J Gastroenterol. 2011 Mar-Apr; 17(2): 124–128. 9 Feliciano DV. Do perforated duodenal ulcers need an acid-decreasing surgical procedure now that omeprazole is available? Surg Clin North Am. 1992;72(2):369– 380 10 Mukhopadhyay M, Banerjee C, Sarkar S, Roy D, Rahman QM. Comparative study between omentopexy and omental plugging in treatment of giant peptic perforation. Indian J Surg; 2011; 73(5):341–345 11 Schein M: Perforated peptic ulcer; in (ed.): Schein’s Common Sense Emergency Abdominal Surgery. Part III. Berlin, Springer, 2005, pp 143–150. 12 Jordan PH Jr. Proximal gastric vagotomy without drainage for treatment of perforated duodenal ulcer. Gastroenterology 1982; 83: 179–183 13 Lal P, Vindal A, Hadke NS. Controlled tube duodenostomy in the management of giant duodenal ulcer perforation: a new technique for a surgically challenging condition. Am J Surg 2009 Sep;198(3):319-23

APPROACH TO MANAGEMENT OF ANASTOMOTIC BREAK DOWN AFTER OESOPHAGECTOMY Taole Mokoena D Phil FRCS

Introduction

Original practice of oesophagectomy for cancer was to perform an anastomosis intra- thoracically (Ivor-Lewis). Anastomotic break down in the thorax is associated with very high morbidity and mortality(1,2),, thus the move towards placing the anastomosis in the neck (McKeown)(1,2). Although anastomotic break down may be even more frequent in cervical anastomoses, their morbidity and mortality are less severe compared to intra-thoracic break downs(2).

Risk Factors for Oesophagogastric Anastomotic Break Down There are a number of factors that can lead to anastomotic break down, some are technical and others are patient related(2,3,4). The risk factors include preoperative albumin, loss of weight, poor respiratory function, poor nutrition, high intra-operative blood loss, hypoxia and hypotension. The surgeon’s objective should be to minimise the technical factors and optimise the patient’s condition pre-, intra-, and post-operatively to minimise breakdowns(3,15). Uppermost in patient factors is nutritional status.

Definition of Anastomotic Breakdown(2,5)

Anastomotic break down is said to have occurred if there is clinical or radiographic leak demonstrated.

Diagnosis of Anastomotic Leak(3,4,5,6,9)

Anastomotic leak may be diagnosed by:

i. Demonstration of gastro-intestinal contents through the drains. ii. Such leak may be confirmed by letting the patient swallow methylene blue and this comes out through the drain. iii. Contrast study with water soluble material eg urograffin or gastrograffin. Barium should not be used. iv. Contrast CT scan. v. Flexible oesophagogastroscopy which can assess both the extent of anastomosis break down and stomach tube integrity or necrosis.

Pathology of Anastomotic Leak(6,2)

The break down is usually at the oesophagogastric anastomosis, but can also be on the gastric tube “suture” line. If the colon or small bowel was used as the conduit, the break down is at the oesophago-colic or oesophago-intestinal anastomosis respectively. The relative frequency of anastomosis break down is that oesophago-intestinal is least frequent while oesophago-colic is most frequent. However the gastric tube is the most commonly used conduit after oesophagectomy for cancer for its simplicity (2,7,8).

The leak may be contained in the mediastinum or dissipated within the pleural cavity. In the neck, it can also be confined to the area around the anastomosis or effuse through the drain or freely to the atmosphere if accompanied by cutaneous incision wound break down. It can also track down into the superior part the mediastinum. Contained leak may result in abscess formation while free pleural leak may lead to empyema thoracis. 28

Anastomotic breakdown may be early (less than 7 days) or late. Early break down is usually due to technical problems while late breakdown is usually from non-healing or necrosis of the anastomosis.

Effects of Anastomotic Break Down (2,9,10)

Limited and contained leak may have no systemic effects as long as there is no florid sepsis. However if untreated it may lead to abscess formation with ensuing systemic effects. Free pleural leaks nearly always results in systemic effects such as systemic inflammatory response syndrome (SIRS), septicaemia and shock.

Management of Anastomotic Leak(2,5,6,9,10,11)

A. Intrathoracic Anastomotic Leaks

I Contained mediastinal leak

Small contained mediastinal leak many be managed non-operatively with broad spectrum antibiotics and adequate nutritional support. GI fluids must be kept away from the anastomotic site by active suction via NGT.

Large collection leaks will need draining. This can be achieved by percutaneous CT guided drainage (pigtail or similar device).

If the defect is large but not a near total disruption of the anastomosis an endoluminal self-expanding stent may be placed(11,12).

II Free Pleural Leak

Small leaks may be managed conservatively with intercostal tube drainage. GI fuilds should be kept away through NGT suction and feeding should be by jejunostomy (better) if already in situ or TPN.

Large leaks require immediate attention to the anastomotic break down site. If only part of suture line has broken down and there is no associated gastric tube suture line disruption or stomach necrosis a (metal) self-expanding endoluminal stent may suffice. If the anastomotic disruption involves a large part of its circumference or the gastric tube suture line is disrupted or there is necrosis operative management is mandatory. Depending on the presence and extent of necrosis or the general condition of the patient, a debridement and re-suture of the anastomosis could be undertaken. If there is stomach tube necrosis the best option is to debride and staple off the stomach remnant and staple of the oesophageal remnant as well, create a cervical diverting oesophagostomy and place a feeding jejunostomy if this had not been done. The pleural cavity is cleaned of all sepsis or decorticated as necessary. After the patient has recovered from effects of sepsis, continuity is re-established. In practice this may need oesophagogastric jejunal interposition graft or retrosternal colonic cervical oesophagogastric interposition graft.

B. Cervical Anastomitc Leaks

I. Contained leaks

Contained localised leak can be managed conservatively with broad spectrum antibiotics, nasogastric tube suction to removed or prevent intestinal content leakage and nil by mouth. Nutritional support, preferably by feeding jejunostomy if already created or TPN is crucial. If the collection is large this should be drain percutaneously.

II. Free drainage via the neck drain

This is managed by keeping the drain in situ to form a fistula. The fistula should close with adequate nutritional support via feeding jejunostomy.

III. The leak may track down into the superior part of the mediastinum. If the neck drain reaches there, this may suffice. However, if not then a suitable drain should be placed perhaps on high volume low pressure suction pump system. Some have described the use of T-tube designed to create a controlled fistula (13)

IV. Complete disruption or gastric tube suture line disruption or necrosis needs surgical management and revision. If gastric tube necrosis to extensive, this should be take down and the remnant stapled off and the oesophagus brought out as a oesophagostomy for delayed later reconstruction with colon interposition graft.

Prevention and Anticipation of Anastomotic Leaks after Oesophagectomy

Because of the relative frequency of anastomotic leaks after oesophagectomy and their devastating effects especially of the intrathoracic anastomosis, certain anticipatory steps or procedures are undertaken as part of the initial operation.

There is no manner or mechanism by which anastomotic breakdown may be completely eliminated. Stapled and hand sewn anastomoses are accompanied by similar rates of break down(14).

However a few anticipatory steps to minimise the effects of break down or provide effective management are prudent.

1. Nasogastric tube suction for 6-7 days post-op is assured by securing the NGT with nasal halter before the “routine” check contrast oesophagogram.

2. A pyloroplasty is fashioned to allow free gastric fluid drainage into the duodenum. Although gastric drainage is similar whether pyloroplasty was done or not in the long run, during the early phase gastric stasis is experienced due to the inevitable vagotomy that accompanies oesophagectomy. These patient may “vomit” and aspirate during the early phase of oral feeding.

3. A feeding jejunotomy is fashioned as an insurance that should anastomotic break down occur, good enteral feeding may be achieved. Enteral feeding is to be preferred over TPN.

4. Placement of the oesophagogastric anastomosis in the neck is to be preferred since morbidity and mortality after anastomotic break down is less than intrathoracic leak.

Summary

Anastomotic break downs after oesophagectomy may be devastating and associated with significant mortality particularly the intrathoracic anastomosis. Therefore many surgeons including the author, strive to place the anastomosis in the neck. Minor or contained leaks may be managed conservatively with or without direct drainage depending of the size of the collection with antibiotics. Major intrathoracic disruptions may be amenable to endoluminal self-expanding stent placement but near complete break down requires operative management. Surgery in fulminant leaks should follow the principle of damage control and GI continuity postponed until the patient has fully recovered from the inevitable sepsis. Establishment of continuity may entail colon interposition graft . Nutrition is paramount and anticipatory feeding jejunostomy should be fashioned during the intitial operation since enteral feeding is the preferred route.

References

1. D’Amico TA. McKeown esophagectomy. Thorac Dis.2014; 6(S3): S322-S324. 2. Urschel JD. Esophagogastrostomy anastomotic leaks complicating esophagectomy: a review. Am J Surg 1995;169: 634-640. 3. Tabatabai A, Hashemi M, Mohajeri G, et al. Incidence and risk factors predisposing anastomotic leak after transhiatal esophagectomy. Ann Thorac Med 2009;4:197- 200. 4. Kassis ES, Kosinski AS, Ross P Jr et al. Predictors of anastomotic leak after esophagectomy: an analysis of the Society of Thoracic Surgeons general thoracic database. Ann Thorac Surg 2013;96:1919-1926. 5. Guo J, Chu X, Liu Y et al. Choice of therapeutic strategies in intrathoracic anastomotic leak following esophagectomy. World J Surg Oncol 2014;12:402-500. 6. Etoxaniz SL, Reyna JG, Orue JLE et al. Cervical anastomotic leak after esophagectomy: diagnosis and management. Cirugia Espanola (Cir Esp) 2013;91:31-37. 7. Briel JW, Tamhankar AP, Hagen JA et al. Prevelence and risk factors for ischemia, leak and stricture of esophageal anastomosis: colon gastric pull-up versus colon interposition. J Am Coll Surg 2004;198:536-542. 8. Davis PA, Law S, Wong J. Colonic interposition after esophagectomy for cancer. Arch Surg 2003;138:303-308. 9. Al-issa MA, Petersen TI, Taha AY, Shehatha JS. The role of esophageal stent placement in the management of post-esophagectomy anastomotic leak. Saudi J Gastro-enterology 2014;20:39-42. 10. Turkyilmaz A, Eroglu A, Aydin Y et al. The management of esophagogastric anastomotic leak after esophagectomy for esophageal carcinoma. Diseases of the Esophagus 2009;22:119-126. 11. Kanatas AN, Aldouri A, Hayden JD. Anastomotic leak after oesophagectomy and stent implantation: a systemic review. Oncol Rev. 2010.DOI:10.1007/S12156-010- 0045-0. 12. Hünerbein M, Stroszczyski C, Moesta KT, Schlag PM. Treatment of thoracic anastomotic leaks after oesphagectomy with self-expanding plastic stents. Ann Surg 2004;240:801-807. 13. Ichukura T, Kawarabayashi N, Ishikawa K, Ikuta S-I, Mochizuki H. T-tube management of a major leakage of the cervical esophagogastrostomy after subtotal esophagectomy: report of three cases. Surg Today 2003;33:928-931.

14. Honda M, Kuriyama A, Noma H, Nunobe S, FurukawaT. Hand-sewn versus mechanical esophagogastric anastomosis after esophagostomy: s systematic review and meta-analysis. Ann Surg 2013;257:238-248 15. Bartels H, Stein HJ, Siewert JR. Pre-operative risk analysis and post-operative mortality of oesophagectomy for resectable cancer. Br J Surg 1998;85:840-844.

MANAGEMENT OF THE OPEN ABDOMEN (LAPAROSTOME) USING TEMPORARY ABDOMINAL CLOSURE (TAC) Prof Jan P Pretorius

At the outset I would like to refer you to the series of 3 articles on this topic published by our Critical Care group in Wound Healing Southern Africa. Part1. Why and when should the abdomen be left open? Wound Healing Southern Africa 2010;3(2):19-23 Part 2. Temporary abdominal closure and the management of the open abdomen or laparostome Wound Healing Southern Africa 2011;4(1):29-35 Part 3. Management of the grade 3 open abdomen (entero-atmospheric fistula isolation) Wound Healing Southern Africa 2011;4(2):94-102

INTRODUCTION At times it is crucial to leave the abdomen open following surgery for complicated abdominal pathology in critically ill patients. This is not a strategy to be taken lightly as it is a morbid, resource intensive procedure with many high risk complications. Despite surgical decompression patients with abdominal compartment syndrome still have a high morbidity and mortality rate. (1, 2, 3, 4,5) It should always be remembered that opening an abdomen necessitates having an immediate plan in place for a specific form of closure, be it short term, for instance, a modified vacuum dressing (vac pack); of indeterminate term, for instance, skin grafting; or a definitive method of closure such as component separation. The complexities of managing an open abdomen are many and vexing and our approaches continue to evolve rapidly. Many innovations have been devised in an attempt to successfully deal with some of the problems of an open abdomen. These have developed into a concept known as Temporary Abdominal Closure (TAC). TAC is any form of dressing applied to the abdomen after non-suture of the abdominal wall. Well known versions of TAC include Bogota bags, the ABRA abdominal closure system and the modified vacuum dressing (otherwise known as the sandwich dressing or vac pack).

The short term aims of an open abdomen are to relieve intra-abdominal pressure and to achieve source control as in cases of sepsis, haemorrhage and necrosis. During this period protection of the gut against erosion should be prioritized. In patients where primary closure is not possible or is delayed, an intermediate phase develops which can be indeterminate in duration. Fistula formation risk is at its highest during this intermediate phase. In our experience spilt skin grafting (SSG) is the most practical solution to protect exposed bowel at this stage. It is easily accessible, maintains the physiological environment and it eventually allows patients to be managed on an outpatient basis. Patients are able to adapt well to the resulting ventral hernia. Definitive closure is still subject to the controversy of optimal timing. This indeterminate phase can be used to optimize wound maturation, normalize nutritional status and improve muscle function as conditions leading to an open abdomen are often associated with multi-organ failure during the intensive care stay.

The initial choice of abdominal closure type depends largely on the grade of open abdomen and how well it is likely to achieve the correlating goals. Commonly occurring complications used to delineate the grade of open abdomen, and how best to avoid or manage them with the use of appropriate grade dependent closure methods (TAC) will be discussed.

Table 1. Common complications of the open abdomen. LOCAL COMPLICATIONS SYSTEMIC COMPLICATIONS • Adhesions • Derangement of fluid balance o Causes stricture formation • Electrolyte disturbances o Form intra-abdominal • Promotion of a catabolic state loculations • Temperature regulation • Adhesions of viscera to abdominal wall and to other visceral organs make primary closure difficult and precludes subsequent surgery.(7) • Fascial retraction • Abdominal sepsis • Fistula formation(8)

THE IDEAL TEMPORARY ABDOMINAL CLOSURE METHOD

Taking the aforementioned complications into consideration, aim to utilize a dressing method with the following characteristics: (9, 10)

1. The dressing must be readily available and inexpensive. 2. It should be easy to apply and remove, allowing access to the abdominal cavity without delay and without difficulty. 3. Nursing care must not be inhibited by the dressing. 4. It should not damage bowel, fascia or skin with repeated applications. 5. It should maintains the abdominal domain (physiological environment) 6. The dressing should prevent collection of peritoneal fluid, pus or blood, thus allow active clearance of fluid. 7. It should serve a barrier function, preventing evisceration and contamination. 8. Prevent abdominal compartment syndrometlht 9. Prevent fascial retraction and allow for a high rate of subsequent primary fascial closure 10. Prevent fistula formation 11. It must allow fistula(e) isolation if present 12. The dressing should prevent adhesion of viscera to the abdominal wall

PLANNING ONCE THE ABDOMEN IS OPEN

The choice of TAC is never a simple or standard decision. Each grade of open abdomen has specific goals. The dressing used must be best suited to fulfilling these goals. Therefore the appropriate choice of TAC is dependent on the grade of open abdomen. However the patient’s clinical condition may also influence the choice of TAC. Therefore it is crucial to plan the closure method at onset taking into consideration the grade of open abdomen and patient’s clinical condition.

Table 2: Working grades of the open abdomen (10) Grade 1a Clean abdomen without adherence of viscera to the abdominal wall Grade 1b Contaminated abdomen without adherence of viscera to the abdominal wall

Grade 2a Clean abdomen with adherence of viscera to abdominal wall

Grade 2b Contaminated abdomen with adherence of viscera to abdominal wall

Grade 3 Open abdomen with visceral fistula

Grade 4 The frozen abdomen (with or without entero-atmospheric fistulae)

From our experience, the initial management of the open abdomen typically involves short term TAC with the aim of early definitive closure. Early definitive closure is commonly accepted as primary fascial closure of the abdomen within 7days (11). If you foresee abdominal closure within a very short time, for instance within 48 hours, cost vs. benefit of choice of TAC becomes an important consideration. In this case a “non-specific” vacuum dressing is useful, accessible and inexpensive. For management longer than 48 hours a more durable and robust but protective dressing may become necessary.

If closure within 7days is not feasible, short term TAC is planned with the aim of indeterminate-term closure such as autologous split skin grafting (SSG). Grafting is then part of a planned ventral hernia strategy. (10) If the patient’s condition does not reach a stage that allows for repeat surgery, then indeterminate-term closure may effectively become the definitive closure method.

Provided the patient recovers adequately from the initial insult, indeterminate closure may be followed by late definitive closure for example component separation. (12) Adequate nutrition has proved to be a major difficulty during this recovery period and it may take months to years to reach this point. (6) Time for wound maturation is also needed.

Available methods of TAC

Knowledge of the available methods of TAC enables the most appropriate choice to be made.(13)

Making the appropriate choice of TAC can be challenging. Table 3 favours specific negative pressure dressings. From our experience it also appears that the specific negative pressure TAC methods yield the best results. It appears to be superior to the non-specific negative pressure dressing. This can be explained by the fact that specific negative pressure dressing have been adapted to cater for the precise requirements and goals of managing different types of open abdomens.

However, one must acknowledge that in open abdomens where one foresees closure within a short period of time, eg. 48 hours, the cost of using a specific negative pressure dressing may not be warranted and this is an important consideration.

Dressing Grade 1a & b open abdomens

When dressing the grade 1a & b abdomen the aim is to maintain the intra-abdominal environment to such a degree that early primary fascial closure is possible. To achieve this it is crucial to preserve the paracolic gutters (prevent adherence of viscera to abdominal wall) and prevent fistula formation. Added to that, fluids should be drained and sepsis prevented at all cost. Our preference to achieve this is using a commercially available specific type negative pressure dressing.

The dressing typically comprises of 5parts 1. A perforated, visceral sponge drape. This is used to envelop the viscera by extending deep into the paracolic gutters an drains fluid from the gutters and from between loops of bowel. 2. A large oval shaped sponge that fits on top of the exposed viscera and occupying the space between the two edges of the open abdominal wall. 3. A large adhesive drape to create a perfect airtight seal. 4. A connecting device that allows for negative suction and drains away excess fluid. 5. A controlled suction unit with alarms and a translucent, calibrated canister that collects drainage fluid.

If a Grade 1 abdomen is dressed with the aim of primary fascial closure, and this is not achieved within seven days, it is in the interest of general care and cost to revise the planning strategy. There is debate about whether or not continuation of the use of dressings to maintain paracolic gutters lessens the risk of abscess formation. However, it is currently commonly acceptable to change to a Grade 2 specific type negative pressure dressing, as this reduces cost, and allows for easier dressing changes. The patient will also not require as much visceral manipulation, and it is more reasonable to do these dressings outside of theatre, and in an ICU environment.

Table 3: Commonly used temporary abdominal closure (TAC) methods

TAC DESCRIPTION PRO’S CON’S Bogota:3-liter plastic Inexpensive Requires suturing of peri-wound Bogota Bag irrigation bag is emptied Transparent tissue resulting in tissue trauma and cut open so it lies flat Available in the Adherence of bowel to or operating room abdominal wall (14) Silo (X-ray film bag) Ease of application No abdominal stabilization (14) The edges are trimmed Strong and able to Usually results in loss of fascia and sutured to the skin prevent evisceration necessitating subsequent surgical (14) of pendulous viscera. intervention for hernia repair Lack of fluid containment results in overall tissue damage Leakage from under bag can leave bed wet and increase the risk of worsening hypothermia and causes difficult nursing care No opportunity to isolate enteroatmospheric fistula High rate of fistula formation (14) Specifically manufactured Easy access into Expensive Retention for use in laparostomes – abdomen Requires measuring IAP sutures (ABRA) Silicone sheet, abdominal Sutures can be Potential damage to peri-wound wall closure set, tightened at integrity elastomer retainers. sequential dressings No active removal of fluid preventing fascial No protection of visceral integrity retraction (15) High risk of fistula formation Primary fascial Needs to be used in conjunction closure facilitated (15) with another dressing No abdominal stabilization

Wittman Patch 2 Bur Sheets are sutured Prevents fascial No active removal of fluid to opposing fascia to fit retraction Requires measuring IAP the opening Allows stepwise re- No stabilization of internal contents Velcro like approximation of Requires suturing of friable Manual closure via fascial edges fascia tension on the sheet Permits final fascia- Requires additional dressing during dressing change to-fascia closure (16) for maintenance of rectus Reduces the need for abdominus and dermal/epidermal hernia repair (16) reapproximation Allows easy access Lack of fluid containment results in to the abdomen for overall tissue damage further surgical Liner pressure placed on procedures abdominal wall could lead to fascial necrosis Expensive Sepsis (16)

Mesh Closure Variety of products Ease of placement Fistula formation (17) available: absorbable or Re-exploration Rigid and irregular non-absorbable Ability to open and Adherence of mesh to viscera ±Zipper for re-exploration close the abdomen complicating further management. Materials : PP, PTFE, at the bedside Very high rate of sepsis (up to Vicryl® , Marlex, Dexcon® Increased strength 100% reported in some studies) Polyglycolic acid, compared to Bogota Does not allow for fluid removal ® GORE TEX, Composite, Permanent feeding Delayed primary fascial closure Alloderm tube can be placed Expensive (13) Mesh extrusion Damage to surrounding fascia (13)

Non-specific Fenestrated, non- Inexpensive Does not adequately deliver or Negative adherent polyethylene Easy nursing care regulate negative pressure Pressure sheet is placed over the Intended for rapid Swabs become very hard on Dressing (aka viscera and covered with closure negative suction and can be Sandwhich/ moist sterile towels / Re-exploration at injurious conventional sponge eg Ligazano bedside possible Risk of fistula formation negative 2, 10 French silicone Made from common Does not quantify drainage pressure or drains are placed and the materials found in the No alarms compared to regulation Vack Pack) wound is sealed with O.R. provided with V.A.C.® Therapy – adhesive dressing large responsibility on nursing staff Wall suction applied to ensure negative pressure is Sealed with surgical maintained drape Grafting required for closure much of the time Adherence of bowels to fascia probable

Specific Specifically designed for Prevents adhesion of Expensive (13) Negative laparostomy viscera to abdominal Experience of equipment required Pressure Fenestrated, non- wall Learning curve to apply precisely Dressing adhesive dressing Prevents fistula Increased responsibility on nursing covering viscera (between formation (13) staff to ensure constant suction at abdominal wall and Promotes granulation set pressures is maintained viscera) to prepare wound (system is equipped with alarms) Followed by a fenestrated bed. Not translucent sponge Decreased oedema Covered by sterile Clears fluid adhesive drape Provides closed, Negative suction is moist wound healing applied and maintained environment Enhances perfusion Draws wound closed Allows for fistula isolation Protects surrounding fascia (13)

Dressing Grade 2a, 2b and Grade 4 (without fistula) open abdomens When dressing a Grade 2 or a Grade 4 open abdomen, the method and timing of definitive closure will differ from Grade 1a and 1b dressings, due to established adherence of the viscera to the abdominal wall. The goals are to drain fluids, prevent sepsis, prevent fistula formation, and especially to achieve wound bed preparation for split skin grafting, as this is now a priority.

Split skin grafting

Once the wound bed has granulated sufficiently, SSG should be carried out on the wound. This should be done as early as possible, keeping in mind that skin takes to bowel very well, as it is highly vascular. The viscera and the abdominal wall can be grafted separately, or together. The latter can cause a problem with adherence of the graft, as the viscera and abdominal wall move independently of one another with respiration. Vacuum dressing could be applied successfully to the freshly grafted wound. This will keep the graft in place and clear excess fluid, if necessary. Remove this dressing after 4-5 days, or when soiled.

Dressing changes

Dressing changes are governed by the clinical scenario. If a patient still needs procedures in the operating room, such as bowel anastomoses, removal of packs or relook laparotomy, the dressing should be changed in theatre. It will then be carried out as frequently as the procedures are necessary. If a patient only needs simple washouts or inspection, the dressing may be changed in the ICU, provided that appropriate equipment and anaesthesia are available. Changing the dressing every 5-7 days is advised, but if the abdomen is septic, more frequent changing is preferable.

Conclusion

An open abdomen is a difficult situation to manage well. Many different temporary abdominal closure methods have been proposed in an attempt to deal with the morbidity and complications of this condition. In our experience, it appears that specific negative pressure dressings are the most effective form of TAC. They can be adapted to the needs of the various grades of open abdomen, and offer essential, practical advantages. These include fluid removal, the promotion of wound bed granulation, and the prevention of sepsis and fistulation. This promotes successful closure of the open abdomen.

References

1. Mentula P, Hienonen P, Kemppainen E, et al. Surgical decompression for abdominal compartment syndrome in severe acute pancreatitis. Arch Surg. 2010;145(8):764-769. 2. Shapiro MB, Jenkins DH, Schwab CW, Rotondo MF. Damage control: collective review. J Trauma. 2000;49(5): 969-978. 3. Nicholas JM, Rix EP, Easley KA, et al. Changing patterns in the management of penetrating abdominal trauma: the more things change, the more they stay the same. J Trauma. 2003;55(6):1095-1110. 4. Johnson JW, Gracias VH, Schwab CW, et al. Evolution in damage control for exsanguinating penetrating abdominal injury. J Trauma. 2001;51(2):261-271. 39

5. Carlotti AP, Carvalho WB. Abdominal compartment syndrome: a review. Pediatr Crit Care Med. 2009;10(1):115-120. 6. Joels CS, Vanderveer AS, Newcomb WL, et al. Abdominal wall reconstruction after temporary abdominal closure: a ten-year review. Surg Innov. 2006;13(4):223-230. 7. Sutton E, Bochicchio GV, Bochicchio K, et al. Long term impact of damage control surgery: a preliminary porospective study. J Trauma. 2006;61(4): 831-834. 8. Kushimoto S, Miyauchi M, Yokota H, Kawai M. Damage control surgery and open abdominal management: recent advances and our approach. J Nippon Med Sch. 2009;76(6):280-290. 9. Carlotti AP, Carvalho WB. Abdominal compartment syndrome: a review. Pediatr Crit Care Med. 2009;10(1):115-120. 10. Leppaniemi AK. Laparostomy: why and when. Crit Care. 2010;14(2):216-218. 11. Balogh Z, Moore FA, Goettler CE, et al. Management of abdominal compartment syndrome. In: Ivatury R, Cheatham M, Malbrain M, Sugrue M, editors. Abdominal compartment syndrome. Georgetown: Landes Bioscience, 200; p 264-294. 12. Ramirez OM, Ruas A, Dellon AL. Components separation method for closure of abdominal wall defects: an anatomic and clinical study. Plast Reconstr Surg. 1990;86:519- 526. 13. Tieu BH, Cho SD, Luem N, et al. The use of the Wittman patch facilitates a high rate of fascial closure in severely injured trauma patients and critically ill emergency surgery patients. J Trauma. 2008;65(4):865-870. 14. Tremblay LN, Feliciano DV, Schmidt J, et al. Skin only or silo closure in the critically ill patient with an open abdomen. Am J Surg. 2001;182(6): 670-675. 15. Foy HM, Nathens AB, Maser B, et al. Reinforced silicone elastomer sheeting, an improvedmethod of temporary abdominal closure in damage control laparotomy. Am J Surg. 2003;185:498-501. 16. Barker DE, Green JM, Maxwell RA, et al. Experience with vacuum-pack temporary abdominal wound closure in 258 trauma and general and vascular surgical patients. J Am Coll Surg. 2007;204:784-793. 17. Bee TK, Martin A, Croce MD, et al. Temporary abdominal closure techniques: a prospective randomised trial comparing polyglactin 910 mesh and vacuum-assisted closure. J Trauma. 2008;65(2): 337-344.

MANAGEMENT CHALLENGES PRESENTED BY ENTEROCUTANEOUS AND ENTEROATMOSPHERIC FISTULA IN CURRENT PRACTICE B Singh, S Mewa Kinoo, R Naidoo Department of Surgery, University of KwaZulu-Natal and King Edward VIII Hospital, Durban

Introduction

Enterocutaneous fistula (ECF) remains a surgical catastophy that continue to present a formidable challenge in current surgical practice. Until 2 decades ago, issues pertaining to the development and management of ECF had attained a state of laudable clarity, notwithstanding the general absence of Level 1 evidence.1

Advances in critical care together with a greater understanding of fistula pathology, behaviour and outcome have seen the management ECF evolve from an aggressive surgical option to a measured conservative approach. The latter approach, in addition to affording the detection and eradication of lingering intra-abdominal sepsis and correction of nutritional and metabolic imbalances, may expedite the spontaneous closure of ECF. This was prompted by Chapmans report (in 1964) that mortality associated with ECF decreased from 58% to 16% in patients who received more than 1500 kcal/d (largely delivered by the enteral route). Patients administered >3000 kcal/day were reported to have a mortality rate of 12%, and a fistula closure rate approaching 90%. Those patients unable to maintain this caloric intake continued to have a high mortality rate and low fistula closure rate (55% and 37%, respectively).2 ,3

The addition of technical innovations, improvements in diagnostic modalities and the availability of novel therapies to the therapeutic armamentarium of ECF management had led to the reduction in mortality rate for this condition to between 3.5% to 37%. 1, 4, 5

This landscape has been considerably altered in current surgical practice with the wide usage of open abdomen (OA) techniques to address abdominal compartment syndrome. The occurrence of an enteric “fistula” in the midst an open abdomen (OA) is called an “entero-atmospheric fistula” (EAF) - inappropriately because it does not have a fistula tract, the absence of which invariably precludes spontaneous closure of the “fistula”.

The challenges presented by EAF are considerable; the fluid, electrolyte losses with acid– base derangement and sepsis source control are much more challenging compared to ECF, resulting in an unremitting hypercatabolic state. Furthermore, there are difficulties in effective collection of enteric effluent. Spillage of enteric contents of an EAF on the adjacent OA surface continuously impairs the healing process, which aggravates local wound sepsis. These challenges have ensured that the morbidity rates of EAFs are high (compared to ECF). The principles of care for EAF are based on the tenets of ECF management that are sequential:

1. Initial resuscitation 2. Early recognition and management of sepsis 3. Nutritional support 4. Reducing the fistula output 5. Wound care / controlling the fistula 6. Surgical intervention

1. Initial resuscitation This involves the correction of fluid, electrolyte and acid-base imbalances

2. Early recognition and management of sepsis

This involves, source control, drainage of sepsis and antibiotic therapy

3. Nutritional support 6

The patient with an EAF is invariably hypercatabolic due to sepsis associated with an underlying starvation metabolism. The metabolic needs of the patient can be estimated using the Harris-Benedict equations taking into account appropriate modifiers for sepsis and postoperative states. The rate of output from the fistula also greatly affects nutritional needs. The requirements for low-output fistulas range 25 to 30 kcal/kg/d with a protein need of 1.5 to 2 g/kg/d of protein; high-output fistulas may require up to 2 times the overall caloric daily requirement and 2 to 2.5 × baseline protein requirements to achieve a positive nitrogen balance; daily small bowel secretions may contain up to 75 g of protein, material that would ordinarily be reabsorbed.2

Following the correction of fluid and electrolyte and eradication of sepsis, minimizing the fistula discharge and establishing a positive nitrogen balance are crucial. Total parenteral nutrition (TPN), by affording bowel rest and rapid repletion of nutrition, is recommended during this phase of the patient’s management. TPN decrease fistula volume and offers a significant improvement in mortality and fistula closure rates.7

In addition to maintaining gut mucosa, enteral nutrition may also decrease fistula output. The supplementation with immunonutrition has failed to demonstrate improvement in mortality.8, 9

Following the initial period of bowel rest, it is reasonable to advocate enteral nutrition. Adequate nutritive absorption may be feasible with at least 1 – 1.5 meters of functioning small bowel remaining.2

Enteral feeding must be commenced cautiously, with continuous, low volume feeds delivered via soft post-pyloric feeding tube; TPN must be maintained while nutritional goals are sought. For gastric feeding, osmolality is increased slowly to hyperosmolar targets, followed by volume targets. With small bowel feeding (via feeding jejunostomy or postpyloric feeding tube), volume tolerance needs to be achieved first; this may be difficult in the high- output fistula as enteral feeds can increase the volume of fistula output.2

The use of fistuloclysis (feeding into the efferent limb of a fistula), either with enteral formulas or chyme output from the proximal fistula has gained currency (particularly in resource depleted services) and has the appeal of being undertaken at home with little.10,11

4. Reducing ﬁstula output

Reduction of fistula output may be achieved by keeping the patient nil per os and effective drainage of the stomach via a nasogastric tube. TPN affords adequate bowel rest as well as reducing GI secretions. Reduction of GI secretions maybe further achieved by the use of drugs; these include proton pump inhibitors to reduce acid secretion, somatostatin or analogue (octreotide) to reduce enteric and pancreatic secretions (but no evidence to show effect on fistula closure) and drugs that slow intestinal transit time such as loperamide, diphenoxylate, and opioids.

5. Wound care / controlling the fistula 12

Wound care management and the effective collection of the enteric effluent with isolation of the EAF opening and the prevention of the contamination of the adjacent wound are central to the management of the abdominal wound in the patients with EAF. To this end there are several methods available using the principle of negative pressure wound therapy [the “VAC (vacuum assisted closure) systems”] that have been shown to be effective in expediting the management of the OA ;13 Among these methods are the “Floating stoma”14, the “Fistula VAC”15, the “Tube VAC”16, the “Nipple VAC”17 and the “Ring and silo VAC”18 techniques. The challenge presented by EAF in an OA is reflected in desperate technique of Malecot intubation of the EAF and then tunnelling this through adjacent well vascularised tissue to convert an EAF to an ECF19.

While there are anecdotal reports of low output fistulas closing spontaneously following conservative medical treatment and VAC application to the OA, the presence of factors that would

preclude spontaneous closure (such as muco-cutaneous continuity, distal obstruction, length of fistua tract, among other factors) have to be considered when using VAC systems. The value of VAC systems reside in its expediting the healing of the wound around the EAF. 12, 21

The measures described for the management of EAF together advances in critical care and surgical care have ensured that mortality rates have decreased from as high as 70% in the past decades to about 42%.20 The challenge presented by EAF is reflected in it being classified as Grade 3 as per Bjorck’s classification of the OA, wherein Grade 4 is the frozen and inoperable OA. 22

Notwithstanding the value and advances of conservative treatment of ECF and EAF, surgery remains the cornerstone of fistulas that have not closed spontaneously. Definitive surgery for the closure of small bowel ECF or EAF is demanding in terms of the physiological reserves of the patient, surgical technical expertise and hospital resources.

The failure of small bowel ECF or EAF to consistently close spontaneously underscores the need to develop reproducible surgical strategies that would ensure a favourable outcome. However, even in experienced hands, a re-fistulation rate between 9% and 32.9% after definitive surgery has been reported. It is therefore necessary that the surgeon treating patients with small bowel ECF or EAF become facile with surgical strategies and techniques that would ensure a safe and effective procedure.

The resection of the involved enteric loop is the most definite way of treating an ECF or EAF. Surgery should only be undertaken in patients in good general status and free of infection.20 These conditions are possible to attain in some patients as early as 1–2 months,20, 23 while others accomplish this target after 6–12 months or even after a 1-year period24 and will affect the timing of the surgery.

6. The principles of surgical intervention

• With the progressive decrease in fistula output at the 6 week stage, return of bowel activity and restitution of nutritional status, it is reasonable to pursue with conservative treatment with the expectation of spontaneous closure of the fistula. However, fistulas with factors known to prevent spontaneous closure or those persisting for >2 months are unlikely to close spontaneously.1 • The timing of the surgical intervention in relation to the most recently undertaken laparotomy is crucial because it impacts the rate of further complications, Furthermore, dense, vascular adhesions, the legacy of obliterative peritonitis, are most evident between 3 and 12 weeks; surgery during this period may predispose to fistula recurrence. 43

• Gaining safe access into the invariably scared abdomen is facilitated by siting the incision in the sub-xiphoid area where the liver protectively overlies bowel loops. • In mobilising the small bowel, begin in an area considered “hospitable”. Unravel the entire small bowel from the ligament of Treitz to the caecum, thereby unravelling all sites of small bowel obstruction. • Resecting the bowel segment bearing the fistula and repairing, rather than direct suture closure is a principle that has ensured a low rate of fistula recurrence. However, depending on the extent of the fistulous opening and absence of oedema, friability or intrinsic bowel disease (such as inflammatory bowel disease), a wedge resection may be adequate. • During the procedure, the thinned out small bowel is vulnerable to injury by overzealous handling; for this reason the use of bowel clamps is inadvisable. • Apply diligence in ensuring that no iatrogenic perforations are overlooked. • Repair all serosal tears because these may predispose to spontaneous perforation in the context of postoperative ileus or intestinal obstruction these patients are vulnerable to. • Routine stenting of the small bowel has been recommended following repair of the fistula. 1

Conclusion

Although tempting, surgery as primary management for fistula closure without adequate patient optimization is highly unsuccessful. Notwithstanding this approach, adequate patient optimization, remains a long drawn out process and requires patience from both the surgeon and patient. Furthermore while optimizing these patients for eventual surgery, fistulas may close spontaneously negating surgery and the risks associated with it. It is well documented that the success of optimization lies in providing and maintaining an adequate nutrition and preventing sepsis. In the event that a patient requires surgical repair such as in a case of EAFs, strict surgical principles should be adhered to avoid recurrence of fistulas.

References

1. Singh B, Haffejee AA, Allopi L, Moodley J. Surgery for high-output small bowel enterocutaneous fistula: a 30-year experience. International Surgery 2009, 94(3):262-268 2. Dudrick SJ, Maharaj AR, McKelvey AA. Artificial nutritional support in patients with gastrointestinal fistulas. World J Surg 1999;23(6):570–576 3. Chapman R, Foran R, Dunphy JE, Foran R, Dunphy JE. Management of intestinal fistulas. Am J Surg 1964;108: 157–164 4. Haffejee AA, Surgical management of high output enterocutaneous fistula. Curr Opin Clin Nutr Matab Care 2004; 7: 309 -316 5. Li J, Ren J, Zhu W, Yin L, Han J. Management of enterocutaneous fistula: a 30 year clinical experience. Chin Med J (Eng) 2003;116: 171 – 175 6. Bleier JI, Hedrick T. Metabolic support of the enterocutaneous fistula patient. Clin Colon Rectal Surg 2010; 23: 142 - 2015, Volume 45, Issue 9, pp 1102-1111148 7. Lloyd DA, Gabe SM, Windsor AC. Nutrition and management of enterocutaneous fistula. Br J Surg 2006; 93(9):1045–1055 8. Heyland DK, Novak F, Drover JW, Jain M, Su X, Suchner U. Should immunonutrition become routine in critically ill patients? A systematic review of the evidence. JAMA 2001;286(8):944–953 44

9. Marik PE, Zaloga GP. Immunonutrition in critically ill patients: a systematic review and analysis of the literature. Intensive Care Med 2008;34(11):1980–1990 10. Teubner A, Morrison K, Ravishankar HR, Anderson ID, Scott NA, Carlson GL. Fistuloclysis can successfully replace parenteral feeding in the nutritional support of patients with enterocutaneous fistula. Br J Surg 2004;91(5): 625–631 11. Peer S, Moodley MS, Cassimjee HM, Singh B. Fistuloclysis--a valuable option for a difficult problem. S Afr J Surg. 2008; 46(2):56-7 12. Marinis A, Gkiokas G, Argyra E, Fragulidis G, Polymeneas G, Voros D. “Enteroatmospheric fistulae”—gastrointestinal openings in the open abdomen: a review and recent proposal of proposal of a surgical technique 13. Tavusbay C. Use of a vacuum-assisted closure system for the management of enteroatmospheric fistulae. Surgery Today 14. Subramaniam MH, Liscum KR, Hirshberg A. The floating stoma: A new technique for controlling exposed fistulae in abdominal trauma. J Trauma 2002;53:386–388 15. Brock WB, Barker DE, Burns RP. : Temporary closure of open abdominal wounds: The vacuum pack. Am Surg 1995;61: 30–35 16. Al-Khoury G, Kaufman D,Hirshberg A. : Improved control of exposed fistula in the open abdomen. J Am Coll Surg 2008;206:397–398 17. Open Abdomen Advisory Panel, Campbell A, Chang M, et al : Management of the open abdomen: From initial operation to definitive closure. Am Surg 2009;75(11 Suppl):S1–S22 18. Verhaalen A, Walkins B, Brasel K: Techniques and cost effectiveness of enteroatmospheric fistula isolation. WOUNDS 2010;22:212–217 19. Ramsay PT, Mejia VA. : Management of enteroatmospheric fistulae in the open abdomen. Am Surg 2010;76:637–639 20. Becker HP, Willms A, Schwab R. Small bowel fistulas and the open abdomen. Scand J Surg 2007;96:263–27 21. Schein M. What’s new in postoperative enterocutanous fistulas? World J Surg 2008; 32: 336 - 338 22. Björck M, Bruhin A, Cheatham M, Hinck D, Kaplan M, Manca G, Wild T, Windsor A. Classification--important step to improve management of patients with an open abdomen. World J Surg. 2009;33(6):1154-7 23. Marinis A, Gkiokas G, Anastasopoulos G, et al : Surgical techniques for the management of enteroatmospheric fistulae. Surg Infect (Larchmt) 2009;10:47–52 24. Jamshidi R, Schecter WP. Biological dressings for the management of enteric fistulas in the open abdomen: A preliminary report. Arch Surg 2007; 142:793–796.

RECTOVAGINAL FISTULA (RVF) Dr BH Pienaar

The term denotes an epithelial lined tract from the rectum to the vagina. The majority of RVFs will be found in close proximity to the dentate line, either at or just above this landmark. It is important to distinguish a fistula below the dentate line from those proximal to the line as these should be called anovaginal fistula. This aspect is important as the treatment is different.

There are a number of ways in which RFV may be classified namely location, etiology and/or size.

The most practical is probably by location as this would also indicate which approach should be used to address the problem. Perineal approach: This would be used for RFV where the fistula is situated in the lower third of the rectum. Alternatively a low fistula.

Transabdominal approach: This would be used for a fistula which occurs in the middle third of the rectum and posterior vaginal fornix.

Size may be used as a differentiating parameter. 1.Small < .5 cm 2.Medium .5 – 2.5 cm 3.Large > 2.5 cm

Etiology 1. Obstetric trauma (most common) 2. Radiation injury 3. Iatrogenic trauma 4. Neoplasm 5. Inflammatory bowel disease (Crohn’s)

Pathophysiology Obstetric trauma may manifest in different ways where the failure to correct perineal defects or secondary infection of episiotomy may lead to fistula formation. In years gone by prolonged labour with pressure from the foetal head was a major cause of RVF.

Lately the stapled resection procedures performed in the vicinity of the dentate line have been associated with RVF.

Crohn disease often is associated with RVF due to perirectal abscess.

Diverticulitis and/or abscess may result in RVF. The most vexing and difficult to manage are fistulas that result from radiation therapy in pelvic malignancies.

In all conditions but especially the latter previous pelvic surgery, smoking and diabetes increases the risk for the development of fistula.

Other rare causes include tuberculosis, lymphogranuloma venereum.

Symptomatology Faeces and flatus are passed through the vagina. It is often associated with diarrhoea which makes the symptoms worse. Severe vaginitis and cystitis may be the presenting symptom. Rarely patients may be found to be asymptomatic.

The clinical picture may also present as incontinence.

Examination Routine standard examination in the rooms may provide the correct diagnosis. It is important to determine sphincter function at the initial examination.

A simple test is to place a vaginal tampon whilst methylene blue is instilled into the rectum. The tampon can be inspected after 15-20 minutes when the blue discoloration of the tampon will confirm the diagnosis.

Treatment Surgical correction is the only method that may result in complete healing. This may take the form of repair and in some cases diversion by colostomy. Colostomy may be used in repair of recurrent fistulas or post radiation repairs.

Biopsy of the fistula prior to repair is essential.

Anatomy Thorough knowledge of the anatomy in the region is important in order to effect successful repair. The rectovaginal septum is a thin layer of tissue where the perineal body is the most caudal portion of this septum with the anal sphincter complex closely related to the perineal body.

Imaging Barium enema and CT scan may be utilised in conjunction with endorectal and vaginal sonography.

Surgical therapy

Preparation should always include complete mechanical bowel preparation. Some authors recommend poorly absorbable antibiotics such as neomycin. Prophylactic SYSTEMIC antibiotic use is recommended. Local repair 47

Transanal advancement flap repair. (Prone positon & operating anoscope)

The flap consists of mucosa and submucosa. The tract is curetted whilst the fistulous opening in mucosa is excised. The fistula is closed with circular muscle. The flap is sutured in position with interrupted sutures. The vaginal opening of the fistula is left open.

Transabdominal repair

High fistula necessitates this approach especially if complicated by radiation, inflammatory bowel disease and diverticulitis. The affected bowel must be resected. Omentum may be used as an interposition buttressing structure.

Prognosis

Trans-anal advancement flap.

Expects success in 77-100% is reported in different series. It is extremely important that that sphincter repair is performed simultaneously or that it is intact.

Subsequent childbirth should be by caesarean section especially if sphincter repair had been part of the initial procedure.

Recurrent fistula makes subsequent successful repair more difficult and prone to failure. Rectal sleeve advancement may play a role.

Transabdominal procedures Due to the fact that the etiological factors are usually more advanced pathology the outcome is less favourable.

REFERENCES 1. Galandiuk S, Kimberling J, Al-Mishlab TG, et al. Perianal Crohn disease: predictors of need for permanent diversion. Ann Surg. 2005 May. 241(5):796- 801; discussion 801-2. 2. Bangser M. Obstetric fistula and stigma. Lancet. 2006 Feb 11. 367(9509):535-6. 3. Browning A, Menber B. Women with obstetric fistula in Ethiopia: a 6-month follow up after surgical treatment. BJOG. 2008 Nov. 115(12):1564-9. . 4. Bricker EM, Johnston WD. Repair of post-irradiation rectovaginal fistula and stricture. Surg Gynecol Obstet. 1979 Apr. 148(4):499-506. 5. Cohen JL, Stricker JW, Schoetz DJ, et al. Rectovaginal fistula in Crohn''s disease. Dis Colon Rectum. 1989 Oct. 32(10):825-8. 6. Giordano P, Gravante G, Sorge R, Ovens L, Nastro P. Long-term outcomes of stapled hemorrhoidopexy vs conventional hemorrhoidectomy: a meta-analysis of randomized controlled trials. Arch Surg. 2009 Mar. 144(3):266-72. 7. Shobeiri SA, Quiroz L, Nihira M. Rectovaginal fistulography: a technique for the identification of recurrent elusive fistulas. Int Urogynecol J Pelvic Floor Dysfunct. 2009 Jan 22. 8. Gonzalez-Lama Y, Abreu L, Vera MI, et al. Long-term oral tacrolimus therapy in refractory to infliximab fistulizing Crohn's disease: a pilot study. Inflamm Bowel Dis. 2005 Jan. 11(1):8-15. 48

9. Nirei T, Kazama S, Hiyoshi M, Tsuno NH, Nishikawa T, Tanaka T, et al. Successful treatment of rectovaginal fistula complicating ulcerative colitis with infliximab: a case report and review of the literature. J Clin Med Res. 2015 Jan. 7(1):59-61. 10. Laurent S, Barbeaux A, Detroz B, et al. Development of adenocarcinoma in chronic fistula in Crohn's disease. Acta Gastroenterol Belg. 2005 Jan-Mar. 68(1):98-100. 11. Kumaran SS, Palanivelu C, Kavalakat AJ, et al. Laparoscopic repair of high rectovaginal fistula: is it technically feasible?. BMC Surg. 2005. 5:20. . 12. Mukwege D, Mukanire N, Himpens J, Cadière GB. Minimally invasive treatment of traumatic high rectovaginal fistulas. Surg Endosc. 2015 Apr 7. 13. Lamazza A, Fiori E, Schillaci A, Sterpetti AV, Lezoche E. Treatment of rectovaginal fistula after colorectal resection with endoscopic stenting: long-term results. Colorectal Dis. 2015 Apr. 17(4):356-60. 14. Casadesus D, Villasana L, Sanchez IM, et al. Treatment of rectovaginal fistula: a 5-year review. Aust N Z J Obstet Gynaecol. 2006 Feb. 46(1):49-51. 15. Khanduja KS, Yamashita HJ, Wise WE Jr. Delayed repair of obstetric injuries of the anorectum and vagina. A stratified surgical approach. Dis Colon Rectum. 1994 Apr. 37(4):344-9. 16. Jasonni VM, La Marca A, Manenti A. Rectovaginal fistula repair using fascia graft of autologous abdominal muscles. Int J Gynaecol Obstet. 2006 Jan. 92(1):85-6. 17. Ellis CN. Outcomes after repair of rectovaginal fistulas using bioprosthetics. Dis Colon Rectum. 2008 Jul. 51(7):1084-8. 18. Gonsalves S, Sagar P, Lengyel J, Morrison C, Dunham R. Assessment of the efficacy of the rectovaginal button fistula plug for the treatment of ileal pouch- vaginal and rectovaginal fistulas. Dis Colon Rectum. 2009 Nov. 52(11):1877-81. 19. Ulrich D, Roos J, Jakse G, et al. Gracilis muscle interposition for the treatment of recto-urethral and rectovaginal fistulas: a retrospective analysis of 35 cases. J Plast Reconstr Aesthet Surg. 2009 Jan 20. .Schouten WR, Oom DM. Rectal sleeve advancement for the treatment of persistent rectovaginal fistulas. Tech Coloproctol. 2009 Dec. 13(4):289-94. 20. Loffler T, Welsch T, Muhl S, et al. Long-term success rate after surgical treatment of anorectal and rectovaginal fistulas in Crohn's disease. Int J Colorectal Dis. 2009 Jan 27. 21. El-Gazzaz G, Hull T, Mignanelli E, Hammel J, Gurland B, Zutshi M. Analysis of function and predictors of failure in women undergoing repair of Crohn's related rectovaginal fistula. J Gastrointest Surg. 2010 May. 14(5):824- 9. 22. Burke C. Rectovaginal fistulas. Clin J Oncol Nurs. 2005 Jun. 9(3):295-7. 23. Fry RD, Kodner IJ. Rectovaginal fistula. Surg Annu. 1995. 27:113-31. 24. Hilger WS, Cornella JL. Rectovaginal fistula after posterior intravaginal slingplasty and polypropylene mesh augmented rectocele repair. Int Urogynecol J Pelvic Floor Dysfunct. 2006 Jan. 17(1):89-92. 25. Husain A, Johnson K, Glowacki CA, et al. Surgical management of complex obstetric fistula in Eritrea. J Womens Health (Larchmt). 2005 Nov. 14(9):839-44. 26. MacRae HM, McLeod RS, Cohen Z. Treatment of rectovaginal fistulas that has failed previous repair attempts. Dis Colon Rectum. 1995 Sep. 38(9):921-5. 27. Miklos JR, Kohli N. Rectovaginal fistula repair utilizing a cadaveric dermal allograft. Int Urogynecol J Pelvic Floor Dysfunct. 1999. 10(6):405-6. 28. Moore RD, Miklos JR, Kohli N. Rectovaginal fistula repair using a porcine dermal graft. Obstet Gynecol. 2004 Nov. 104(5 Pt 2):1165-7. 49

29. Nowacki MP. Ten years of experience with Parks' coloanal sleeve anastomosis for the treatment of post- irradiation rectovaginal fistula. Eur J Surg Oncol. 1991 Dec. 17(6):563-6. 30. Steichen FM, Barber HK, Loubeau JM, et al. Bricker-Johnston sigmoid colon graft for repair of postradiation rectovaginal fistula and stricture performed with mechanical sutures. Dis Colon Rectum. 1992 Jun. 35(6):599- 603. 31. Tsang CB, Madoff RD, Wong WD. Anal sphincter integrity and function influences outcome in rectovaginal fistula repair. Dis Colon Rectum. 1998 Sep. 41(9):1141-6.

DIFFICULTIES IN THE MANAGEMENT OF BILE DUCT INJURIES AFTER LAPAROSCOPIC CHOLECYSTECTOMY MD Smith

Most surgeons report an increase in cholecystectomies performed especially in the public sector in SA. This reflects a change in incidence of cholecystolithiasis in South Africans, however data confirming this remains limited. There is also limited data in South Africa regarding the magnitude of the CBDI after laparoscopic surgery. This includes the incidence and the management strategies. It is recommended that these cases be centralized to centers with the multidisciplinary skills to manage the problem.

There are a number of consequences of the CBDI that we need to unpack. Firstly the impact of the injury on the patient, the doctor and the medico legal process. There is clear evidence today that CBDI does have a long term impact on the patient in terms of quality of life and even a suggestion that there may be an impact on long term survival. Even a well done timeous repair has consequences. Long term stricture formation of the anastomosis is well described at about 10%.

With rising medico-legal claims the legal process needs to be explored. For patients to receive some form of compensation in SA law, there must be a finding of negligence. The implications are that an adverse event is always a consequence of negligent behavior on the part of the doctor. While surgical misadventure is nearly always present there is good evidence today that this is not commensurate with negligence. There is an impact on the surgeon during the process of litigation including significant stress, anxiety and even an impact on productivity due to a loss of self-esteem during the legal process hinged on negligence. A change in this legal structure may allow a less adversarial resolution for both the patient and the surgeon. It is however worth noting that often the legal culpability resides in issues of adequate consent and the appropriate management of the patient once the injury has occurred.

Is there something that can be done to reduce the incidence of CBDI? The literature is clear that improved training and better intraoperative strategies can reduce the incidence of CBDI. Psychomotor studies have shown that there are normal human errors brought into play which are not in themselves negligent. Better training and greater experience in laparoscopic training is required. A recent paper in the SAJS demonstrated a significant lack of laparoscopic equipment in training institutions reducing the supervised training of registrars. Data showing a greater incidence amongst less experienced surgeons supports this argument.

Strasberg and colleagues have described an operative strategy that has now been evaluated in a number of studies with a real reduction in the incidence of CBDI. This approach relies on better dissection of the anatomical structures in Calots triangle considered to be the ‘Critical view of safety”. This approach is possible in the majority of patients and when not possible it should be an indication to convert the procedure to an open laparotomy for safe completion of the cholecystectomy. Conversion should not be seen as failure by the surgeon but rather one of a number of ways to prevent CBDI. Others include subtotal cholecystectomy, preoperative prediction of difficult cholecystectomies and

the increased use of cholecystostomy in the severely inflamed Gallbladder. Predictors of the difficult cholecystectomy become less obvious as the skills of surgeons improve. Previous predictors no longer routinely apply however the presence of an impacted stone in Hartman’s pouch compressing the common hepatic duct (Mirizzi syndrome) is still considered a contraindication to LC. However obesity, cirrhosis and acute cholecystitis no longer constitute absolute contraindications. The training of registrars needs to ensure that all these approaches are well taught. In a recent fellowship exam this question was asked with the expectation that all candidates would understand the implication of this technique, yet the response was poor This suggests that there is a deficit in the training of registrars.

There are a number of other recommendations that remain controversial. The role of intraoperative cholangiograms (IOCG)remains a topic of debate. Two broad approaches are described; IOCG has not proven to reduce the incidence of CBDI especially when performed on demand. Its routine use is probably more appropriate to identify undetected CBD stones and the information regarding the anatomy probably does not prevent CBDI. There are those who believe that routine on table Cholangiograms will reduce the incidence. Most centers in SA do not practice routine IOCG.

It is well recognized that only symptomatic cholecystolithiasis requires cholecystectomy. After the introduction of Laparoscopic cholecystectomy and the acceptance that this was the standard of care, the numbers of cholecystectomies reported globally increased. It was thought that this was due to a relaxation in the indications for the procedure. Patients and health professionals must accept the current guidelines for cholecystectomy; only symptomatic or complicated gallstones should be treated by cholecystectomy.

A high index of suspicion for CBDI in patients who do not display an appropriate clinical response in the immediate post-operative period, is essential to early diagnosis. The global incidence of injuries detected post operatively, as opposed to intraoperative identification, remains high. The complex management of patients with delayed diagnosis, is responsible for a significant component of the high cost as a result of increased need for ICU, more investigations longer hospital stay and in many studies reflects the patients at risk for mortality.

There is good evidence to support the early referral of these patients to centers able to manage patients who require interventional radiology and advanced surgical skills. The training of surgeons must stress the appropriate initial management of these patients before referral to these centers. Preventing biliary peritonitis by adequate drainage of bile is far more important that the immediate repair of the injury. This does not require expert skills rather an awareness of the need for adequate drainage. Once this has been established early transfer before expensive investigations such as MRCP, CT scanning or endoscopy is important. This may result in some unnecessary transfers but overall this may improve the outcome for patients who require the skills of the experienced centers.

Strasberg A or D injuries can both be managed with endoscopic interventions. These patients should be included in the generic strategy for the recognition and management of CBDI.

There is no doubt that we can do better in the prevention of CBDI following laparoscopic cholecystectomy. The strategy must involve all agencies involved in training, assessment and accreditation. The Minister of Health has recently identified the need to address the rapidly rising number of medico-legal claims and is clear that all these agencies need to participate in addressing this trend in the best interests of patients but also to prevent depletion of scarce resources available to the health sector. We should all revisit our training programs and ensuring that everyone plays their part in the overall prevention and management of these patients to reduce the consequences to the patient and to reduce the health expenditure.

Recommended reading

1. Steven M. Strasberg. Avoidance of biliary injury during laparoscopic cholecystectomy. J Hepatobiliary Pancreat Surg (2002) 9:543–547 2. Andersson R, Eriksson K, Blind PJ, Tingstedt B. Iatrogenic bile duct injury--a cost analysis. HPB (Oxford) 2008; 10(6): 416-419. 3. Anandalwar SP, Choudhry AJ, Choudhry AJ, Svider PF, Van Luven C, Ahlawat S, et al. Litigation in laparoscopic cholecystectomies. Am Surg 2014; 80(6): E179-81. 4. Landman MP, Feurer ID, Moore DE, Zaydfudim V, Pinson CW. The long-term effect of bile duct injuries on health-related quality of life: a meta-analysis. HPB (Oxford) 2013; 15(4): 252-259. 5. Sakorafas GH, Milingos D, Peros G. Asymptomatic cholelithiasis: is cholecystectomy really needed? A critical reappraisal 15 years after the introduction of laparoscopic cholecystectomy. Dig Dis Sci 2007; 52(5): 1313-1325. 6. R. Matthew Walsh, MD, J. Michael Henderson, MD, David P. Vogt, MD, and Nancy Brown, RN. Long-term outcome of biliary reconstruction for bile duct injuries from laparoscopic cholecystectomies. Surgery 2007;142:450-7. 7. SM Strasberg, LM Brunt. Rationale and the Use of the Critical View of Safety in the Laparoscopic Cholecystectomy. J Am Coll Surg2010;1: 132-137 8. RM Vazquez. Common sense and common bile duct injury: common bile duct injury revisited. Surg Endosc 2008;22:1743-1745 9. SR Thomson, MD Smith. Minimising the 'cost' of laparoscopic cholecystectomy. SAMJ 2015;105:6

POST-HEPATECTOMY LIVER FAILURE Dr C Jeske, Department of Surgery, University of Pretoria and Steve Biko Acadmic Hospital

Introduction

Post-hepatectomy liver failure represents a major source of morbidity and mortality after liver resection. It is considered to be a devastating complication with little treatment other than vigilant supportive care. The incidence of post-hepatectomy liver failure ranges from 4- 19%.1-5 In recent literature, the incidence is less than 10%, owing to improved preoperative assessment and intraoperative and postoperative management.6,7 Several studies report a lower rate of PHLF is East Asian countries at 1-2%. Mortality following partial hepatectomy in the past two decades still ranges from 0 to 6%, however, and PHLF has been implicated as contributing to mortality in the majority of cases.8

Definition

An excess of 50 studies have defined PHLF. This wide variety of definitions among groups have made comparison of rates between studies challenging.9-12 The time period in which liver failure is defined is also contentious, some using 3 days others 7 days. Prior to this decade there has been no uniform definition of PHLF. A more widely accepted recent definition is that of the International Study Group of Liver Surgery (ISGLS). In 2011 they defined PHLF as the “impaired ability of the liver to maintain its synthetic, excretory and detoxifying functions, which are characterized by an increased international normalized ratio and concomitant hyperbilirubinemia (according to the normal limits of the local laboratory) on or after postoperative day 5.” The ISGLS group also advocated a grading system in which laboratory values, clinical symptoms, and need for increasingly invasive treatments define severity of PHLF (see Table 1).9

Table 1. ISGLS definition and grading of PHLF.(9) Grade Clinical Treatment Diagnosis Clinical symptoms Location for A Deterioration in None 1. UOP >0.5 None Surgical ward liver function mL/kg/h

B Deviation from Non-invasive: fresh frozen 8. UOP ≤0.5 32. Ascites Intermediate expected post- plasma; albumin; diuretics; mL/kg/h • Weight gain unit or ICU operative course non-invasive ventilatory • BUN <150 mg/dL • Mild respiratory without support; abdominal • <90% O2 saturation • Confusion despite oxygen requirement for ultrasound; CT scan supplementation invasive • INR ≥1.5, <2.0 procedures

C Multi-system Invasive: hemodialysis; • UOP ≤0.5 mL/kg/h • Renal failure ICU failure requiring intubation; extracorporeal • BUN ≥150 mg/dL • Hemodynamic invasive treatment liver support; salvage • ≤85% O2 saturation Instability despite high fraction of • Respiratory failure hepatectomy; inspired oxygen support vasopressors; intravenous glucose for hypoglycemia; ICP monitor

ISGLS, International Study Group of Liver Surgery; PHLF, post-hepatectomy liver failure.

The ‘50-50 criterion’ (PT <50% and bilirubin >50 µmL/L on post-op day 5) have been proposed to predict post-hepatectomy mortality.10 There are also comprehensive algorithms for predicting PHLF. Others have proposed a peak total serum bilirubin of greater than 7mg/dL.11 Table 2 summarizes current post-operative predictive models of PHLF.

Despite efforts by the ISGLS to define PHLF more accurately to predict prognosis early after hepatectomy, several studies have questioned the accuracy of the ISGLS criteria. Skrzypcyk et al. compared the ISGLS definition with the ’50-50 criteria’ and peak bilirubin >7 mg/dL criteria among 680 patients who underwent either minor or major hepatectomies.13 The ISGLS definition was found to be least predictive of both the occurrence of major complications (positive predictive value of 49.2% for ISGLS vs. 78.9% for ’50-50 criteria’ and 65% for peak bilirubin >7 mg/dL), as well as the risk of post-operative death (OR=6.9 for ISGLS vs. OR=21.1 for ’50-50 criteria’ and OR=21.7 for peak bilirubin >7 mg/dL).13

Table 2. Predictive models of PHLF

Postoperative Models Description

MELD Score A scoring system used for determining the gravity of end-staged liver disease. Takes into account serum creatinine, bilirubin, INR, and dialysis status.

Child-Pugh Score Child-Pugh scoring system is developed for grading liver cirrhosis into three distinct classes. Takes into account serum bilirubin, albumin, INR, ascites, and encephalopathy.

The 50–50 criteria state that a combined prothrombin time less than 50 % and a serum bilirubin of 50-50 Criteria10 more than 50 μmol/L on POD 5 is a significant predictor of postoperative mortality due to PHLF.

Kim et al. proposed the 50–50 criteria to be adjusted to the combination of PT <65 % and bilirubin Kim et al.14 ≥38 μmol/L on POD 5.

Snap peak bilirubin>7 A postoperative peak bilirubin greater than 7 mg/dL was found to be a significant predictor of death mg/dL11 as a result of liver failure.

ISGLS Definition9 The ISGLS proposed the general definition of a postoperatively acquired deterioration in the ability of the liver to maintain its synthetic, excretory, and detoxifying functions, characterized by an increased INR and hyperbilirubinemia on or after postoperative day 5. To be divided further into grade A, B, or C.

A composite integer-based risk score based on international normalized ratio, bilirubin, creatinine, Hyder et al.12 and complication grade at POD 3.

MELD, model of end-stage liver disease; INR, international normalized ratio; POD, postoperative day; PHLF, post-hepatectomy liver failure; ISGLS, International Study Group of Liver Surgery.

Risk Factors

Identification of risk factors for PHLF is critical to help identify patients most at risk of developing PHLF and to develop strategies aimed at decreasing the incidence and mortality associated with PHLF. Independent risk factors can be categorized into three main categories: patient-related, liver-related, and surgery/postop-related factors (Table 3).

Patient-related factors

These include age, male gender, malnutrition, diabetes, and American Society of Anesthesiology (ASA) score. Some studies had implicated older age as a risk factor for PHLF; however other studies have documented the safety of liver resection in the elderly. Animal studies have suggested a loss of the liver’s regenerative capacity, as well as impaired liver function with increased age.15-18 Aldrighetti et al, Nanashima et al and Kim et al have all failed to detect a difference in age-related PHLF in their studies.19-21

Diabetes, either alone or in combination with metabolic syndrome, has also been associated with greater risk of PHLF. The association of diabetes with risk of PHLF may be due to the important role insulin plays in the regulation of hepatocyte function and regeneration. Specifically, a lack of insulin has been noted to cause hepatic atrophy in animal models.22 Furthermore, 80% of peri-operative deaths in diabetic patients were secondary to PHLF. Excess mortality seen in diabetic patients undergoing major hepatic resection is likely multifactorial, with alterations in liver metabolism, decreased immune function, and hepatic steatosis contributing to post-operative liver dysfunction.24

Liver-related Factors Table 3. Risk factors for PHLF

Patients undergoing hepatectomy present with a wide Patient-related factors range of underlying hepatic parenchymal disease including Age (>65 years) cirrhosis, steatosis, steatohepatitis, and chemotherapy Male gender induced liver injury that can affect the ability of the liver to regenerate after liver resection. Metabolic disorders

Cirrhosis is a major consideration when operating on Preoperative chemotherapy patients, especially in the hepatocellular carcinoma (HCC) Sepsis Malnutrition population. Animal models have demonstrated that after ASA score resection, cirrhosis is associated with decreased levels of hepatocyte growth factor, impaired transcription factors, Liver- related factors and a reduction of DNA synthesis, leading to lower Grade of the tumour volumes of regenerated liver.25,26 In patients with Hepatitis cirrhosis, PHLF rates range between 2% and 19%.27-34 Child-Pugh score and Model for End-Stage Liver Disease Portal venous pressure (MELD) may give some information about the degree of Cirrhosis cirrhosis, they may underestimate the ability of a patient to withstand resection. In these patients preoperative Cholestasis

tests for functional liver reserve, such as Indocyanine Surgery- related factors Green clearance (ICG), are considered essential.35 Complex operations

As neoadjuvant and conversion chemotherapeutic Extent of resection strategies improve, the percentage of patients undergoing liver resections after exposure to chemotherapy is General surgical models increasing.36 Common regimens for the treatment of colorectal cancer include 5-fluorouracil combined with Large blood transfusion oxaliplatin, irinotecan, and the targeted agents bevacizumab and cetuximab. Although these regimens Left hepatectomy have helped to make previously unresectable metastases resectable, their prolonged use can result in steatosis, Duration of Pringle Maneuvre steatohepatitis, and sinusoidal congestion. Several studies have associated sinusoidal injury and steatohepatitis with compromised liver regeneration as well as increased morbidity following hepatic resection.37-40

Surgery-related Factors

In addition to patient-specific factors, the performance of the surgical procedure itself influences risk of PHLF in both the immediate postoperative period and in a delayed manner. Intraoperative blood loss and transfusion requirements have been associated with an increase in postoperative complications following hepatectomy.41,42 Postoperative blood transfusions required due to intraoperative blood loss, results an immunosuppressive effect that may contribute to PHLF.43 58

An important surgery-related factor is the extent of resection and avoidance of ‘small-for- size’ liver remnant following hepatectomy. Small for size livers are associated with an increase in severe graft dysfunction with increased hepatocyte injury, hyperbilirubinemia, prolonged PT, portal hypertension, and ascites.44-46 Efforts should be taken preoperatively to predict adequate future liver remnant (FRL) in an effort to decrease the risk of PHLF. In patients for whom <25% of the pre-operative liver volume is left post-resection, the risk of PHLF is 3 times that of patients with >25% of liver volume remaining.47

Preoperative Risk Assessment

Given the high mortality and morbidity rate associated with PHLF, there has been great interest in techniques to preoperatively identify patients at high risk for hepatic dysfunction or failure. There are multiple different techniques available to evaluate the quality and quantity of the FLR and hence the risk for developing PHLF.

Quality assessment of the liver

Traditional liver function markers and clinical scoring systems

Two tools used widely for assessment of liver function are the Child-Pugh score and the MELD score.48,49 Both scoring systems were originally developed to grade chronic liver disease and cirrhosis in liver transplant candidates; however, both are currently also used to screen patients preoperatively for the risk of PHLF as well as to evaluate perioperative liver function.48,50,51 Patients with advanced Child-Pugh B and C scores are not candidates for hepatectomy due to their risk of PHLF. Child-Pugh classification falls short in predicting PHLF-related mortality in the more modest to mild cirrhosis patients.52 The MELD model has similarly been extensively evaluated with mixed results.49,52-54

Indocyanine Green Retention at 15 min (ICG-R15)

ICG is a water-soluble, nontoxic fluorescent dye that is injected intravenously and is eliminated almost exclusively by the liver. The absorption and emission spectrum of ICG are both in the near infrared range allowing for measurements to be performed by non-invasive monitoring.8,55-62 The ICG-R15 test has been shown to predict more accurately PHLF compared with both the Child-Pugh classification and MELD model.63,64 There is however no clear consensus on the cut-off value for ICG-R15 allowing for safe hepatic surgery and while the test is used in the east, its adoption has not been widespread in western centers. Some studies suggest a cut off of 14% and others report higher cut-off values in relatively younger patients of 17%.65,66

Other Liver Function Tests for the Quality Assessment

Other qualitative tests based on the principle of clearance of substrate by the liver include substances such as lidocaine, galactose, aminopyrine, amino acid, and methacetin.48,67-70 None have been proven to be superior to ICG-R15 for the prediction of PHLF or PHLF- related mortality.63 There are also tests based on the synthetic functions of the liver such as serum levels of hyaluronate and type IV collagen, energy production of the liver, and the number of receptors for asiaglycoprotein (GSA scintigraphy).71-79 The high cost and complexity of these tests has limited their clinical implementation to date.

Quantity Assessment of the Liver

Preoperative assessment of the FLR size after hepatectomy is fundamental for effective and safe hepatic resection. Currently, there is no uniform consensus regarding the limit of the FLR volume necessary to achieve a ‘safe’ liver resection or the modality most effective for evaluating FLR size preoperatively.80 The techniques most frequently used to assess FLR 59

include computed tomography (CT) and magnetic resonance imaging (MRI).81 CT and MRI both show excellent accuracy and precise quantification of hepatic volume.82-84 Additionally, careful evaluation of preoperative CT imaging should focus on liver attenuation, indicating steatohepatitis, as well as splenomegaly, varices, ascites, or consumptive thrombocytopenia, to raise suspicion of underlying cirrhosis.

Strategies to Prevent PHLF

Treatment of PHLF hinges first on its prevention. The preventive techniques are applied to those patients identified to be at risk of PHLF based on the preoperative assessment as outlined above, i.e. those patients deemed to be at high risk based on underlying patient factors, presence of cirrhosis, preoperative laboratory values, volume of liver to be resected or estimated FLR after resection.

Most preventive strategies have been aimed at increasing the FLR.85,86 Techniques aimed at increasing the FLR are portal vein embolization (PVE), portal vein ligation (PVL) and associating liver partition and portal vein ligation for staged hepatectomy (ALPPS) procedure. PVE is an ultrasound-guided percutaneous procedure that induces liver hypertrophy following embolization of the portal vein ipsilateral to the side of the disease, it thus leads to hypertrophy of the contralateral side, i.e. the FLR. Additionally, it results in an increase in the production of hepatic growth factor and tissue growth factor, along with redistributing the portal blood flow to the FRL. CT volumetry should be performed 3-4 weeks after PVE to assess the degree of hypertrophy. PVE allows for hypertrophy of 30-40% in 80% of patients within 4-6 weeks.87 Current guidelines recommend PVE for patients with underlying cirrhosis and an anticipated FLR of ≤40%, or patients with normal liver function and intended FLR of <20%.88

In some circumstances a PVL may be preferable, especially when resecting a bilobar malignant liver lesion which requires a two-stage approach due to inadequate FLR volume.89,90 At the first operation the contralateral portal vein is ligated and in 3-6 weeks after adequate hypertrophy has taken place, the second stage is performed. At which time the extended/major hepatectomy is performed. A meta-analysis reported that there was no statistically significant difference comparing PVE and PVL in terms of increasing FLR volume, morbidity and perioperative mortality.91

The ALPPS procedure was developed to decrease time between PVL and resection for patients with borderline FRL volume.92 ALPPS may facilitate superior hypertrophy of the FLR compared with PVE, with a reported 74% volume increase of the remnant liver in a mean of 9 days. This procedure has however been reported to have high operative morbidity (16- 64% of patients) and perioperative mortality (12-23% of patients).93

Treatment of Post-hepatectomy Liver Failure

When present PHLF is manifest by progressive multi-system organ failure, including renal insufficiency, encephalopathy, need for ventilator support, and need for pressor support. As hepatic function worsens, patients develop persistent hyperbilirubinemia and coagulopathy.93 Patients need to be closely monitored postoperatively to identify and treat PHLF as early as possible. Particular attention should be paid to early clinical and laboratory signs of liver failure including changes in coagulation factors and bilirubin, as well as signs of encephalopathy. Patients should also be monitored for early signs of infection, hemodynamic failure, renal failure, malnutrition, or metabolic disorders.94,95 Patients should be monitored in an ICU setting.

The management principles follow those of the American Association for the Study of Liver Diseases (AASLD) for the management of acute liver failure.96 The severity of the PHLF 60

needs to be followed using laboratory values. Resuscitative measure and organ support provide the optimal environment for liver regeneration.

It is necessary to detect and treat all triggers or aggravating factors of PHFL at a very early stage: establishment of an appropriate antimicrobial therapy (blood, ascites and bile samples), looking for vascular complication (arterial or venous thrombosis), radiological drainage if biliary fistula, optimization of vital functions (vascular filling in case of hypovolemia) and prevention of malnutrition by enteral or parenteral nutrition (needs increased by 30%, supplementation with vitamins and trace elements). The use of hepatotoxic and nephrotoxic drugs should be banned. Regarding the symptomatic treatment, the use of lactulose is usually recommended to correct encephalopathy, and administration of mannitol is possible to reduce intracranial hypertension. Compensation in platelets or clotting factors is needed in case of coagulopathy.

The development of artificial liver brought much hope in terms of treatment in fulminant hepatic failure. For the management of PHLF, few studies have been conducted, and results are disappointing since no survival improvement was found, but it may be helpful as a bridge to possible orthotopic liver transplantation (OLT).97,98

The most efficient treatment of PHLF remains OLT. This indication however is marginal due to graft shortage and the oncologic context in which most of these procedures are performed. PHLF accounts for less than 10% of liver transplantations. OLT for PHLF has only been sparsely reported.99,100 The initial indication for hepatic resection frequently involves a malignancy outside of transplantation criteria.

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CHALLENGES IN THE MANAGEMENT OF GASTROSCHISIS AND EXOMPHALOS Dr E Müller

Abdominal wall defects are divided into omphalocele and gastroschisis. While often considered together, they are distinct and separate entities.

Embryology and Aetiology

The current understanding of the aetiology for an omphalocele suggests that this defect is not from a failure in body wall closure or migration. It is thought that an omphalocele develops due to a failure of the viscera to return to the abdominal cavity. Other intra- abdominal viscera often found in the omphalocele sac are liver, stomach, ovary and testis. The sac consists of covering layers of the umbilical cord and includes amnion, Wharton’s jelly, and peritoneum. The location of the defect is in the mid-abdomen, but may also occur in the epigastric or hypogastric regions as well.

The aetiology for gastroschisis is less clear. Currently, the ventral body fold theory, which suggests failure of migration of the lateral folds (more frequent on the right side), is most widely accepted. Due to increasing incidence of gastroschisis, there are a number of possible causative factors including tobacco, lower maternal age and low socioeconomic status. Gastroschisis occurs in 1 in 4000 live births. An increased incidence in mothers younger than 21 years has been widely documented. There is also a significant increase in incidence in all age groups over the past two decades. Preterm delivery is more frequent compared with babies without an abdominal wall defect.

Pre- and perinatal management

Gastroschisis: In the developed world, most gastroschisis children are diagnosed sonographically by 20 weeks gestation. Detection of freely floating bowel loops and a defect in the abdominal wall to the right of the umbilical cord are diagnostic. Intrauterine growth retardation is common in these foetuses. Some authors advocate selective preterm delivery based on the finding of bowel distention and thickening of the bowel wall on prenatal ultrasound. Studies in animal models have shown that the duration of amniotic fluid exposure is correlated with the degree of inflammatory peel seen on the bowels. Damage to the pacemaker cells and nerve plexi may be the reason for the profound dysmotility and malabsorption seen in these patients. Early delivery may mitigate these effects, but the literature is mixed. Currently available evidence does not support elective preterm delivery for gastroschisis.

Neonatal Resuscitation

Neonates with gastroschisis have significant evaporative water losses from the open abdominal cavity and exposed bowel. Appropriate intravenous access should be obtained and fluid resuscitation initiated after birth. Nasogastric decompression is important to prevent further gastric and intestinal distention. The neonate should be positioned on the right side to prevent kinking of the mesentery with resultant bowel ischemia. The bowel should be wrapped with plastic wrap or the infant placed partially in a plastic bag to reduce evaporative losses and improve temperature homeostasis. Although gastroschisis most often is an isolated anomaly, thorough examination of the neonate is important. In addition, the bowel must be carefully examined for intestinal atresia, necrosis, or perforation. Recent evidence suggests that excess fluid resuscitation is detrimental and results in oedema, an increase in time to closure, and an increased risk of abdominal compartment syndrome.

The primary goal is to return the viscera to the abdominal cavity while minimizing the risk of damage due to trauma or increased intra-abdominal pressure. The two most commonly used treatment options are placement of a silo followed by serial reductions and delayed closure, or primary closure. In all cases, inspection of the bowel for obstructing bands, perforation, or atresia must be undertaken. Primary closure is the preferred option if the bowels can be returned to the abdominal cavity without causing abdominal compartment syndrome. The urinary bladder pressure measured via the inserted urinary catheter should not be higher than 25cm water after closure of the abdominal wall.

Preservation of the umbilicus is preferred because of its superior cosmetic result. In the mid- 1990s, a prefabricated silo was developed with a circular spring that is positioned under the fascial opening, without the need for sutures or general anaesthesia. This has made it possible to insert the silo in the delivery room or at the bedside. After placement, the bowel is reduced daily into the abdominal cavity as the silo is shortened by sequential ligation. When the intestines are entirely reduced, the silo bag is removed and the remaining abdominal wall defect covered by a dressing and left to close by secondary intention. This process takes usually one to two weeks.

Management of associated intestinal atresia

Up to 10% of neonates with gastroschisis have an associated atresia, most commonly jejunal or ileal. These atresias can be treated at the time of abdominal wall closure with resection and primary anastomosis in cases where there is minimal inflammatory peel. If the condition of the bowel makes primary anastomosis inadvisable, the bowel is reduced with the atresia intact and repair is undertaken four to six weeks after the initial abdominal wall closure. If perforation is found, the perforated segment can be resected and a primary anastomosis performed if the inflammation is minimal. Alternatively, an ostomy can be created followed by ostomy closure at a later date. There is no consensus about the optimal management for these complicated problems. Patients with an atresia are considered to be ‘complex’ to differentiate them from the patients without any such association (simple).

Postoperative course

Most authors note worse outcomes with complex cases. Gastroschisis is associated with abnormal intestinal motility and nutrient absorption, both of which gradually improve. Introduction of enteral feeding is often delayed for weeks while awaiting return of bowel function. During this waiting period, nasogastric decompression and parenteral nutrition is required. When bowel activity occurs, enteral feeds can be started and slowly advanced. Because progression to full enteral feeding can take weeks, central venous access is important.

Long term outcomes

Long-term outcomes for patients born with gastroschisis are generally excellent. The presence of complex disease is the most important prognostic determinant for a poor outcome.

Most gastroschisis patients have some degree of intestinal nonrotation. This is typically not repaired at the time of closure and does not have the same incidence of midgut volvulus as other causes of malrotation. However, the parents should be cautioned regarding bilious emesis and instructed to take urgent action if that occurs.

Cryptorchidism is associated with gastroschisis in 15–30% of cases. Several retrospective analyses have shown that placement of the herniated testis into the abdominal cavity will

result in normal testicular descent into the scrotum in most cases. Most centres recommend allowing a year for spontaneous descent and then performing an orchiopexy if needed.

Omphalocele

The diagnosis of omphalocele can be made by ultrasound at the time of the normal 18-week ultrasound evaluation. It is also useful in the detection of other abnormalities which are frequent in these children: Cardiac and central nervous system abnormalities might have a serious impact on prognosis and raise questions about early termination of pregnancy.

The route of delivery is usually vaginal except in giant omphaloceles where C-section is preferred. After delivery, a thorough search for associated anomalies is important. All neonates should undergo an echocardiographic evaluation. Renal abnormalities can be detected by abdominal ultrasound. Neonatal hypoglycaemia should alert the practitioner to the possibility of Beckwith–Weidemann syndrome.

Infants with an omphalocele do not have as significant fluid and temperature losses as those with Gastroschisis. The sac itself can be covered with saline-soaked gauze and an impervious dressing to minimize these losses. An NG tube should be inserted and placed to suction.

Surgical management: Defects that are less than 1.5 cm in diameter are referred to as hernia of the cord and are repaired shortly after birth without any issues as long as there are no associated anomalies. The defects that are larger, but still easy to close without much loss of abdominal domain can also be closed soon after birth. Primary closure consists of excision of the sac and closure of the fascia and skin over the abdominal contents. If the sac is too large for primary closure we prefer nonoperative techniques. The sac is painted with an antiseptic, allowed to slough off and eventually granulation tissue forms on the intestines. From the edges of the wound skin epithelium grows in until the defect is covered by skin. At about age 1 year the abdominal cavity has enlarged enough to be able to receive the intestines from the ventral hernia which is repaired with or without mesh.

MALDESCENDED TESTIS IN ADULTS Dr. Evelyn M Moshokoa, HOD Urology

What it is?

Cryptorchidism/Undescended testis is the absence of one or both testes in normal scrotal position . Clinical evaluation may refer to palpable cryptorchid testes or to nonpalpable testes, which are either cryptorchid or absent.Hidden or obscure testis/testes that may iether be present in an abnormal position or absent.

How common it is?

Epidermiology Cryptorchidism is the most common genital disorder encountered in paediatrics. • 1% to 4% of full-term and • 1% to 45% of preterm male neonates (Sijstermans et al, 2008) Spontaneous descent is more likely and may occur later in premature infants. Spontaneous descent after the first year of life is uncommon.

Gonadal descend Trans abdominal descent 1. Differential growth of vertebrae and pelvis. 2. Enlargement of gubernaculum pulls developing testes toward inguinal region * Insl3 cause gubernaculum enlargement 3. Regression of cranial suspensory ligament * Androgen cause regression of cranial suspensory ligament

Between 10 – 15 weeks testes near future inguinal region

Retractile and Acquired Undescended Testes Theories: • Presence of a fibrous remnant of the processus vaginalis that tethers or foreshortens the cord over time or mobility of the testis within an open sac. • Testis is incompletely descended from birth. (Barthold and Gonzalez, 2003) • Somatic growth results in relative widening of the distance between testis and scrotum. (Redman, 2005; Agarwal et al, 2006).

Genetic Susceptibility • Genetic studies of cryptorchidism suggest that the disease is heritable but that susceptibility is likely polygenic and multifactorial. • Autosomal dominance with reduced penetrance probable mode of inheritance • Recurrence risk ratio (RR) was 10.1 in twins, 3.5 in brothers, and 2.3 in offspring and were significantly higher in maternal than in paternal half-brothers. (Schnack et al, 2008).

An adult is not a big child!

Presentating History • Pain • Hernia • Testicular malignancy • Infertility • Micropenis • Delayed puberty

Hypogonadism • Loss of libido ( desire ) • Fatigue / depression / loss of well-being • ↓ Lean body muscle and mass • ↑ Visceral fat / mass • Sleep disturbances • ↓ Virility • ↑ Sweating / dry skin / anaemia • Osteoporosis

Approach • History • Exam • Investigations • Management

An Adult with empty scrotum Congenital Acquired

• Undscended Torsion

• Retractile Orchidectomy

• Ectopic • Vanished • DSD • Agenesis

Clinical Examination • Palpable • Non – Palpable • Unilateral • Bilateral • Associated penile abnormality • No penile abnormality

Evaluation – Role of Sonar – Baseline investigations ? – Testosterone – Semen analysis • To do a biopsy or not

Anatomy

• Inguinal canal long and developed

• Cremasteric muscles thicker

• Pampiniform plexusmore developed

• Testicular size

Physiology

• Testosterone production

• Spermatogenesis

• Thermoregulation dependence

– Countercurrent mechanism

– Cremasteric reflex

Cryptorchism is the most common disorder of sexual differentiation

Orchiolysis is a common paediatric procedure performed world wide

Laparoscopically introduced in 1976 by Cortes

Diagnostic

Therapeautic

Laparoscopic orchiolysis 74

• Advantages of laparoscopic orchiolysis

Contraindications

• Previous extensive pelvic surgery

Laparoscopic findings

Unilateral

• Absent testis and cord structures

• Absent testis with cord structures exiting the inguinal canal

• High testis

• Testicular Nubbin

– Orchidectomy

Bilateral

• Fowler Stephens

• Prentis Maneuvre

• Orchidectomy

Laparoscopy

• Undescended non palpable testis

• Relative

– Redo cases. Can be done

– Concomitant hernia repair

Adults !

• Modifications have been discussed regarding orchiolysis

• Challenge on mobilization

• Adult with bilateral undcended testis!

– Intra-abdominal testis

– Fowler -Stevens

– When to do orchidectomy?

– When to do nothing?

Absent testis 75

• Treat the complications

• Hypogonadism

– Testosterone supplement

• Family interest

• Self image

– Testicular prosthesis

COMPLICATIONS AND SEQUELAE OF INGUINAL HERNIA REPAIR Prof Zach Koto, Department of Surgery, Sefako Makgatho Health Sciences University

Introduction Inguinal hernia repair one of the most commonly performed operations in surgery worldwide. The concept of watchful waiting which was initially thought of as a viable strategy has now been largely abandoned by most as data shows that on follow-up majority of these so- called asymptomatic patients do eventually need surgery. The Lichtenstein repair which epitomizes tension free repair has over the years become the bench mark against which all types of repairs are measured. The advent of laparoscopic surgery has now become a much preferred procedure that achieves the similar objectives of a tension free repair with comparable recurrence rates. The take up of laparoscopic repair has been low in many centres but the incidence of laparoscopic repair is on the rise.

Complications Complications following hernia repair are very diverse and for purposes of this overview, I will onlydiscuss those complications that are associated with laparoscopic repair. The anaesthetic and general complications will not be discussed here but only procedure related and long term complications.

Procedures related complications

Complications related to anatomy Although knowledge of anatomy of the pelvis is crucial to understanding how vital associated structures are linked to the inguinal defect. This anatomy can be very challenging even to the most experienced of surgeons. In some instances even an obvious hernia can be missed by the uninitiated resulting in no repair at all.

Injury of the surrounding structures The key landmarks should be observed at all times to avoid dissecting in the wrong plane which can result in injury to Iliac vein – this can be a catastrophic complication which can result in significant blood loss and even mortality, This complication must be divided at all costs. In the unlikely event that this happens, the surgeon must apply pressure immediately with a grasper – avoid suction – a swab introduced trough a 10 mm port to apply pressure is helpful, an increase in the pneumoperitoneum pressure is also helpful and immediate conversion of the patient to open procedure must be done.

The key to avoiding this injury is identification of the landmarks and knowing at all times where you are dissecting in relation to the iliac vessels.

Bladder injury Urinary bladder must always be emptied before an inguinal hernia is done laparoscopically – a urinary catheter may be helpful but it is associated with discomfort and possible urinary tract infection. We prefer to empty the bladder before we start the operation by asking the patient to go to the bathroom just immediately before surgery. The insertion of the suprapubic port must be done under vision and meticulous dissection is key. Knowing where you are is crucial during the dissection.

Cord structures Identification of cord structures and the hernia sac is important. The cord structures must be handled with care and one must avoid direct handling of the cord structure to avoid injuring

the testicular vessels and lymphatics. The sac must be dissected meticulously off to avoid injury. The vas and cord structures must be separately identified. The vas is more susceptible to injury because it lies more medial and can be accidentally transected when dividing the sac. It is thus very key to dissect as far medially as possible to identify the vas.

Testicular atrophy Testicular atrophy and necrosis as a result of ischaemic orchitis is a well-recognised complication following an inguinal hernia repair. Although it is reported rarely it does occur. The reported incidence is about 0,5% for primary open inguinal surgery and 5% for recurrent open inguinal hernia (1).

For laparoscopic inguinal hernia repair some investigators report 1% incidence of testicular atrophy. This complication is thought to be more common in open repair. The possibility of this complication must be discussed with the patient beforehand.

The nerves There are four crucial nerves in the posterior abdominal wall that can be injured during a total extra-peritoneal (TEP) hernia repair.

Ilio-inguinal nerve, illiohypogastric nerve that lie on quadratus lumborum muscle, lateral cutaneous nerve of the thigh that runs between the quadratus lamorum muscle and psoas muscle, and genito-femoral nerve that runs on psoas muscle.

These nerves when injured can result in sensory loss of the affected area or chronic groin pain which can be quite incapacitating.

Injury to these nerves can be avoided by avoiding placement of tackers posteriorly unless fixating the mesh or better still using fibrin glue as a fixation strategy.

Chronic inguinodynia Post hernia repair, groin pain is expected for up to 2 months after the procedure. It becomes chronic groin pain if it persists beyond 3 months after the operation. It certainly can be a challenge to manage when it occurs. The management of this condition is a whole separate discussion and will not be discussed here.

Seroma Seroma following a laparoscopic hernia repair is fairly common. It can sometimes be mistaken as a recurrence. Compression of the groin may help reduce this complication.

Haematoma The incidence of haematomas following groin hernia surgery is fairly common. Meticulous dissection and haemostasis is important to minimize this complication.

Mesh sepsis Mesh sepsis is very uncommon. Mesh sepsis can be minimized by avoiding implantation of the mesh in potentially contaminated area. In the unlikely event of mesh sepsis, exploration of the mesh can be avoided by the use of light weight mesh with a large mesh size.

Summary Complications of inguinal hernia repair can be minimized or completely avoided by attention to details meticulous technique and adequate proctoring.

References

1. Neumayer L, Giobbie-Hurder A, Jonasson O, et al. Open mesh versus laparoscopic mesh repair of inguinal hernia. N Engl J Med 2004; 350:1819-1827 2. Wantz G E. Complications of inguinal hernia repair. Surg Clin North Am 1984; 64:287-298 3. Wantz G E. Testicular atrophy as a sequela of inguinal hernioplasty. Int Surg 1986; 7(3):159-63 4. Phillips E H, Arregui M, Carroll B J, et al. Incidence of complications following laparoscopic hernioplasty. Surg Endosc 1995; 9(1):16-21

SURGICAL CONTROVERSIES SYMPOSIUM 3 & 4 OCTOBER 2015 Problems of continence following surgery for haemorrhoids: surgical misadventure or unavoidable complication Dr Stephen Grobler, Bloemfontein

General introduction Pelvic floor and proctologic disorders are commonly encountered in surgical practice. Although regarded as routine pathology by many, choosing the right treatment at the right time can pose a real challenge to the treating surgeon and often involves choosing between two evils. Radical treatment leads to good symptom control but is likely to result in functional deterioration, whereas less invasive treatment is safe but often leads to inferior results. This has been the core problem in the treatment of pelvic floor and proctologic disorders for centuries. The close interaction between the anatomy and physiology of the rectum and anus is responsible for this compromise the surgeon often has to make. Historically functionality was of secondary importance to healing of the disorder, but nowadays it is considered unacceptable to cause permanent disability for a benign disorder. Many classic surgical therapies such as anal stretching and lateral internal sphincterotomy for anal fissure, haemorrhoidectomy and (extensive) lay-open procedures for anal fistula have been re- evaluated over the past decades with special respect to postoperative functionality. Reports of high rates of impaired continence, severe postoperative pain and high rates of recurrence have boosted the incentive to introduce new techniques in the field of proctology. Anatomical considerations The rectum constitutes the last 12-15 cm of the large bowel and starts at the level of the promontory. It is situated within the pelvic cavity. The anal canal is the last part of the rectum, starting at the anorectal junction where the rectum passes through the levator muscle, ending at the anal verge. The length of the functional anal canal is about 4 cm, whereas the anatomical anal canal, extending from anal verge to dentate line is only 2 cm in length. The most important contributor to faecal continence is the anal sphincter, which consists of 2 muscular components: the internal anal sphincter (IAS), 0.3-cm to 0.5-cm thick continuation of the circular smooth muscle layer of the rectum and the external anal sphincter (EAS), 0.6- cm to 1.0-cm thick conjunction of the levator ani muscle complex. Morphologically, both sphincters are separate and heterogeneous. The IAS is a predominantly slow-twitch, fatigue- resistant smooth muscle. The IAS generates mechanical activity, with a frequency of 15 to 35 cycles per minute and ultra-slow waves at 1.5 to 3 cycles per minute. The IAS contributes approximately 70% to 85% of the resting sphincter pressure, but only 40% after sudden distension of the rectum and 65% during constant rectal distension. Thus, the IAS is chiefly responsible for maintaining anal continence at rest. The anus is normally closed by the tonic activity of the IAS. This barrier is reinforced during voluntary squeeze by the EAS. The puborectalis muscle forms a flap-like valve that creates a forward pull and reinforces the anorectal angle. Anal Endovascular Cushions The anal canal is lined with squamous epithelium below the dentate line, and columnar epithelium above. The dentate line is also marked by the lower end of the columns of Morgagni, where the ducts of the anal glands terminate. A substantial number of these glands branch out into the intersphincteric plane. Between the upper border of the anal canal and the dentate line lie three vascularised cushions. The blood-filled vascular tissue and submucosa of the anal mucosa play an important role in producing a more perfect closure of the anus. The internal sphincter ring is unable to close the anal orifice completely – this is filled by the anal cushions, which may contribute 10% to 20% of resting anal pressure by 80

physically acting as a sealing ‘plug’.

Pathophysiology of evacuatory disorders The cause of faecal incontinence is usually multifactorial. Faecal incontinence occurs when the normal anatomy or physiology that maintains the structure and function of the anorectal unit is disrupted. Disruption or weakness of the EAS can cause urge-related or diarrhoea-associated faecal incontinence. Obstetric trauma, the most common cause of anal sphincter disruption, may involve the EAS, IAS and pudendal nerves, singly or in combination. It remains unclear why most women who sustain obstetric injury in their 20s or 30s typically do not present with faecal incontinence until their 50s. In contrast, damage to the IAS muscle or the anal endovascular cushions may lead to a poor seal and an impaired sampling reflex. These changes may cause passive incontinence or faecal seepage, often under resting conditions. Both sphincters may be defective in many patients. The extent of muscle loss can influence the severity of incontinence. Damage to the endovascular cushions may produce a poor anal “seal” and an impaired anorectal sampling reflex. The ability of the rectum to perceive the presence of stool leads to the recto-anal contractile reflex response, an essential mechanism for maintaining continence. Anal leakage caused by mild passive faecal incontinence or soiling is not exclusively caused by diminished sphincter function. On the contrary, dysfunction of evacuation of stools may be the main cause. Many patients with obstructed or dyssynergic defecation have passive faecal incontinence, sometimes accompanied by faecal soiling, due to the incomplete evacuation of stools. They generally loose stools or liquids passively during walking without noticing. Incomplete evacuation of stools in obstructed defecation can be caused by rectocoele or internal and external rectal prolapse. Excessive pelvic floor descent on straining may lead to progressive damage to the striated anal sphincter muscle and or pudendal nerves due to repeated stretch injury. Anal endosonography has shown that aging was associated with an increase in the thickness and echogenicity of the internal sphincter muscle. The sacral nerves are intimately involved with the maintenance of continence. Bowel contents are periodically sensed by anorectal sampling, the process by which transient relaxation of the IAS allows the stool contents from the rectum to come into contact with specialized sensory organs. The likely role of anal sensation is to facilitate discrimination between flatus and faeces and the fine-tuning of the continence barrier. Rectal sensitivity may be too low to detect the presence of residual faeces. Pudendal neuropathy can diminish rectal sensation and lead to excessive accumulation of stool, causing faecal impaction, mega-rectum and faecal overflow. The puborectalis muscle plays an integral role in maintaining the anorectal angle. Its nerve supply is independent of the sphincter. Diarrhoea and constipation with overflow incontinence must be managed to achieving controlled evacuation of stools. The consistency, volume and frequency of stool and the presence or absence of irritants in stool may also play a role in the pathogenesis of incontinence. In the presence of large volume liquid stools, which often transit the hindgut rapidly, continence can only be maintained through intact sensation and a strong sphincteric barrier. Similarly, in patients 81

with bile salt malabsorption, lactose or fructose intolerance or rapid dumping of osmotic material into the colon, the colonic transit is too rapid for both gaseous and stool contents and can overwhelm the continence mechanisms. A variety of medical conditions and disabilities may predispose to faecal incontinence, particularly in the elderly, e.g. immobility and lack of access to toileting facilities. Several medications may inhibit sphincter tone, e.g. anticholinergics, some of which are used to treat urinary incontinence and detrusor muscle instability, muscle relaxants such as baclofen and antispasmodics. In contrast, stimulants such as caffeinated products, fibre supplements, or laxatives may cause diarrhoea.

Haemorrhoidal disease Haemorrhoidal disease is a frequently occurring entity and constitutes the most common proctologic disorder (prevalence 4 – 10%). Haemorrhoids are highly vascular tissue in the submucosal space in the anal canal. Haemorrhoidal tissue gives rise to symptoms such as bleeding, prolapse or pruritus when it slides downward. Aetiological factors are multifactorial and include prolonged straining, irregular bowel habits and heredity. When conservative treatment like dietary- and defaecation habit advice fails, the primary treatment of choice should be is rubber band ligation (RBL). This procedure is reported to be successful in 65-85% of the patients. The setback is that treatment often needs to be repeated in order to be successful and that grade 3 to 4 haemorrhoids are less amenable to banding. This leaves a substantial group of patients which are not treated sufficiently. Doppler-Guided Haemorrhoidal Artery Ligation (DGHAL) or Transanal Haemorrhoidal Dearterialisation (THD) uses custom proctoscopes combined with a Doppler transducer to identify the haemorrhoidal arteries (originating from the superior rectal artery) for selective ligation and fixation. The theory that haemorrhoids occur when there is an imbalance in the blood flow of the haemorrhoidal plexus, either caused by increased inflow or decreased venous outflow underlies the inflow reduction by arterial ligation, causing the vascular plexus to recede. Overactivity of the anal sphincter in patients with haemorrhoids may be primary or secondary and thus raise the notion of the need for anal dilatation or lateral internal sphincterotomy in addition to the surgical treatment of haemorrhoids. Tonic contraction of the sphincter muscle in patients with advanced stages of haemorrhoids is considered by many authors as a primary cause. The nefarious practice of Lord’s stretch is banned to the annals of iniquity! Some operators tend to complete haemorrhoid surgery with lateral internal sphincterotomy (LIS). Sequelae of lateral internal sphincterotomy cannot be excluded and may later negatively affect patient’s anal continence. Overactivity of the anal sphincter in patients with haemorrhoids seems rather to be a secondary phenomenon and therefore there is no indication for lateral internal sphincterotomy (LIS). The pathogenic circle is broken by therapy of the haemorrhoids. Persisting hypertension of the anal sphincter after Milligan-Morgan haemorrhoidectomy may be associated with delayed healing of extensive defects of anorectal mucosa. Postoperative pain leads to increased tension of the anal sphincter and subsequently prolongation of operative wound healing. However, stapled haemorrhoidectomy significantly reduces resting anal pressures in the immediate postoperative period, allowing more rapid improvement in anorectal function compared to Milligan-Morgan haemorrhoidectomy. Anal dilation or lateral sphincterotomy may result in permanent incontinence due to 82

fragmentation of the anal sphincter apparatus. Only mild dilatation of the anal canal is ever allowed. Dilatation should never exceed 40mm (~ 2 fingers or 4 clicks of standard Park’s anal dilator). But even mild dilatation of a stenotic anal canal or pelvic floor weakness may unmask underlying anal sphincter defects and render your patient incontinent, if not immediately, then when they become older! If in doubt, do NOT dilate but rather refer for objective colorectal assessment (ultrasound, physiological testing) and colorectal specialist management. Classic haemorrhoidectomy (“open” Milligan-Morgan, or the preferred “closed” Ferguson) is still an effective procedure for resolving haemorrhoidal symptoms but further affects the already altered anal anatomy and may result in disordered defaecation. There is no doubt that haemorrhoidectomy may endanger the sphincters. This is usually due to inadvertent stripping of the internal sphincter together with the haemorrhoidal complex. Technical errors (ignorance, unfamiliarity and over exuberance) may even damage the external sphincter. Pathology reports of 16% of specimens containing muscle fibres (80% smooth and 20% striated muscle) are cause for concern! It seems that surgical anatomy needs to be included as an important syllabus while educating surgeons for haemorrhoid surgery. Anal endosonography may reveal sphincter defects after haemorrhoidcerctomy– the pattern is usually specific, with patchy disruption of the IAS, but some have EAS defects too. Nevertheless 70% of patients may be asymptomatic, without complaints. (Pre)-existence of small sphincter defects without symptoms should be realized when evaluating patients to decide on causation. There is no excuse for “blind” surgery – get help, learn, train and teach. Ample safe and effective anorectal retractors are available and should be used. Blind mass resection of haemorrhoids by clamping energy devices is also not safe. These energy devices should rather be used to provide haemostasis and cutting of carefully dissected mucosa and submucosa only. Therefore, other techniques have been developed to treat patients that have not reacted to conservative treatment, rubber band ligation or HAL. The Procedure for Prolapse and Haemorrhoids (PPH) or stapled haemorrhoidopexy (SH) entails stapled transanal mucosectomy by circumferential resection of mucosa and submucosa above the haemorrhoids. PPH/SH is reported to be an effective and safe alternative for surgical haemorrhoidectomy with less postoperative pain, shorter hospital stay and greater patient satisfaction. Devastating complications from misplacement of the purse-string in relation to the dentate line (too high) and the depth of biting (too deep bites) and the drawing in of too much tissue into the stapler housing have been reported. The basic notion is that the submucosal purse- string suture should be placed at a distance of 4 - 5 cm above the dentate line; the stapling line should lie 2 to 3 cm proximate to the dentate line. Key technical factors must be respected: - ensure correct positioning of the dilator to facilitate visibility of the whole dentate - tighten the purse-string firmly on the anvil and address the stapler so as to parallel the rectal axis (if firm tightness is not feasible, the procedure is converted to an open haemorrhoidectomy) - precise synchronicity of a progressive introduction of the stapler and the closing of its jaws can sufficiently control the amount of rectal mucosa and submucosa to be resected - check the vaginal wall before engaging the stapler to correct the actual direction of the instrument and safeguard against a possible rectovaginal fistula 83

- the staple line should be checked and defects should be repaired - perform double stapled or custom stapled resections for selected grade IV haemorrhoids, anal- or rectal prolapse - excision of haemorrhoidal components that have failed to shrivel after PPH/SH so as to ensure a more radical result and to relax anastomotic tightness - routinely excise concomitant skin tags or redundant anoderm. Soiling (17-28%), prolapse (3-9%), and incontinence and urgency (1.8-5.6%) have been reported after PPH/SH, but usually improve with time. Persisting incontinence is rare. Complications after using different devices are comparable. The anal dilator for introducing/using the stapling device (diameter 37 mm) could be responsible for the observations. Supposed mucosal resection may excise upper portions of the sphincters if placed too low. Endoanal ultrasound lesions of the internal anal sphincter may be detected.

ANASTOMOTIC FAILURE IN COLORECTAL SURGERY: HOW CAN WE REDUCE THE RISK? Prof Paul Goldberg

Anastomotic failure is an inevitable consequence of performing an anastomosis. There are only 2 causes of anastomotic failure, inadequate surgical technique or incorrect surgical judgement. The surgeon is directly responsible for all anastomotic failures.

The consequences of anastomotic failure may vary from a patient who has a mildly prolonged postoperative recovery to overwhelming sepsis with multiple reoperations and a high mortality. In addition, anastomotic leakage in rectal cancer surgery is associated with worse long term bowel function and increased local recurrence rates with reduced survival (Mirnezami, Mirnezami et al. 2011)

What is an anastomotic leak? There are at least 29 different definitions in the literature. A reasonable definition comes from the International Study Group of Rectal Cancer (Rahbari, Weitz et al. 2010). They defined an anastomotic leak as a defect in the intestinal wall at the anastomotic site leading to a communication between the intra and extra-luminal compartments. They graded leaks as:

Grade A: Leaks that do not change patient management

Grade B: Leaks that require intervention but not re-laparotomy

Grade C: Require repeat laparotomy

Incidence: Reported leak rates for colorectal surgery vary widely from 1%(Paun, Cassie et al. 2010) to 50%(Goligher, Graham et al. 1970) depending on how they are detected and the site of the anastomosis. The closer the anastomosis is to the anus in rectal surgery, the higher the leak rate. A clinical leak rate of around 10% for coloanal anastomosis is generally accepted, but for more proximal anastomoses, leak rates should not be any higher than 1 to 2%.

Defunctioning proximal to an anastomosis with a colostomy or ileostomy does not appear to alter leak rates, but it does decrease the morbidity of a leak (Huser, Michalski et al. 2008, Montedori, Cirocchi et al. 2010). It however adds to morbidity and mortality by adding a second operation for closure.

Factors affecting leak rates • Technical factors: a. Leak rates vary between surgeons. b. Meticulous technique c. No tension d. Good blood supply e. No contamination f. Single layer better than double layer g. Lower leak rate for stapled anastomosis h. Appropriate suture material

i. High IMA ligation

• Management factors: a. Peri-operative hypotension b. NSAIDs c. Over use of perioperative fluids d. Inotropes e. Long operation time f. Blood loss g. Transfusions

• Patient factors a. Emergency surgery b. Significant pre-operative weight loss c. Low albumin d. Obesity e. Diabetes f. Liver disease g. Renal failure h. Myocardial infarction i. Cardiac failure j. Peripheral vascular disease k. Cerebrovascular disease l. Dementia m. Chronic pulmonary disease n. Any tumour o. Immunosuppression i. Steroids ii. Other causes p. Crohn’s disease q. Peritonitis

The important questions a surgeon needs to ask when performing an anastomosis are:

1. How important for the patient is this anastomosis? 2. What is the likely chance of a leak in this patient? 3. Does the patient have the reserve to survive a leak should it occur?

On re-operating or a patient who has had a leak, a surgeon has to establish the cause of the leak. If it is due to a technical error and there is little contamination, it may be reasonable to re do the anastomosis. In most other situations, the surgeon has to change the approach and take the anastomosis down.

References:

Goligher, J. C., et al. (1970). "Anastomotic dehiscence after anterior resection of rectum and sigmoid." Br J Surg 57(2): 109-118.

Huser, N., et al. (2008). "Systematic review and meta-analysis of the role of defunctioning stoma in low rectal cancer surgery." Ann Surg 248(1): 52-60.

Mirnezami, A., et al. (2011). "Increased local recurrence and reduced survival from colorectal cancer following anastomotic leak: systematic review and meta-analysis." Ann Surg 253(5): 890-899.

Montedori, A., et al. (2010). "Covering ileo- or colostomy in anterior resection for rectal carcinoma." Cochrane Database Syst Rev(5): CD006878.

Paun, B. C., et al. (2010). "Postoperative complications following surgery for rectal cancer." Ann Surg 251(5): 807-818.

Rahbari, N. N., et al. (2010). "Definition and grading of anastomotic leakage following anterior resection of the rectum: a proposal by the International Study Group of Rectal Cancer." Surgery 147(3): 339-351.

COMPLICATIONS OF PERIANAL ABSCESSES AND THOSE OF THEIR MANAGEMENT Prof OD Montwedi

• Perianal abscess remains a common surgical problem • Incident high in males

ETIOLOGY

A: TRAUMA penetrating

Local trauma (Abrasions)

B: Local Infection

• Hair follicle • Haemorrhoid • Fissure • Post OP (Sphincterotomy) • Other diseases ( Chron”s disease)

• C: CRUPTOGLANDULAR THEORY

• 1.Perianal , 2 Ischiorectal ,4 Submucus , 5 Marginal ,6 Supralevator , 7Intersphincteric • Management 88

Incision and Drainage

PRINCIPLES

• Criss cross incision over an area of maximal fluctuation • Break all loculations • Packing/ no packing • Antibiotics only for certain situations • Post operative sitz bath • Dressings/ no dressings

COMPLICATIONS

• This can occur before or after surgery • PREOPERATIVE COMPLICATIONS • 1 Rupture with subsequent recurrences or fistula formation • 2 Necrotising fasciitis • common in immune compromised patients • Upward spread of infection along skin , subcutaneous tissue , fascia and muscles • Occurs in about---- of patients • Diagnosis requires a high index of suspicion • Rapid spread, tissues necrosis, excessive pain, no classical signs of inflammation

PRINCIPLES OF MANAGEMENT

• Resuscitate the patient • Antibiotics: Broad spectrum • Surgery: Aggressive debridement with faecal and urinary diversion • Hyperbaric oxygen: shown to help but not a substitute for surgery • Prognosis: Depends on severity. Can be as high as 70% in diabetic patients.

POST OPERATION COMPLICATIONS

IMMEATIATE

A. Bleeding : Rare, but if it does occur simple packing is adequate B. Inadequate drainage C. Missed abscesses: In case of horse shoe abscess or submucus abscess D. Recurrent abscesses/ fistula This remains a common complication. Occurs in crypto glandular abscesses

PREVENTATIVE STRATEGIES FOR RECURRENCES / FISTULAS

• Antibiotics with incision and drainage (No evidence to support this) • Combination of medical therapy for chron”s diseases and prolonged seton use • Fistulotomy at same time with incision and drainage 89

• Plus swab during incision and drainage and fistulotomy in same hospital admission if GIT bacteria are cultured

MANAGEMENT OF FISTULA

1.) DEFINE ANATOMY? CLASSIFICATION (Parkes Classification)

• A.) Superficial • B.) Intersphincteric • C.)Transsphinceteric • D.) Suprasphincteric • E.)Extrasphincteric • 2.) Fistulotomy/ Fistulectomy

3.) Preservation of sphincter function

4.) Post operative wound care

METHODS OF ASSESSING FISTULA

• Palpation • Probes • Injection: H2O2, methylene blue

IMAGING

• Endo anal u/s • CT • MRI 90

• Fistulography

Surgical option

• Fistulectomy: simple, intersphincteric • Fistula plug (collagen plus) Less success rate • Fibrin glue : recurrence high, Procedure can be repeat • Seton: Transsphincteric, suprasphincteric • Flap advancement • Colostomy: chron’s disease • Ligation of intersphincteric fistula tract(LIFT)

E. INCONTINANCE

Incontinence following treatment of perianal abscesses is rare

Increase incidence:

: Repeated drainage for recurrences

- Fistulectomy done same time as drainage - Patients with necrotising fasciitis

REFERENCES

A randomized prospective trial of endoscopic ultrasound to guide combination medical and surgical treatment for Crohn's perianal fistulas. Spradlin NM, Wise PE, Herline AJ, Muldoon RL, Rosen M, Schwartz DA. Am J Gastroenterol. 2008 Oct;103(10):2527-35. doi: 10.1111/j.1572-0241.2008.02063.x. Epub 2008 Aug 5. PMID: 18684178 [PubMed - indexed for MEDLINE]

Treatment of perianal sepsis and long-term outcome of recurrence and continence. Stremitzer S, Strobl S, Kure V, Bîrsan T, Puhalla H, Herbst F, Stift A. Colorectal Dis. 2011 Jun;13(6):703-7. doi: 10.1111/j.1463-1318.2010.02250.x. Epub 2010 Mar 11. PMID: 20236152 [PubMed - indexed for MEDLINE]

Does adjuvant antibiotic treatment after drainage of anorectal abscess prevent development of anal fistulas? A randomized, placebo-controlled, double-blind, multicenter study. Sözener U, Gedik E, Kessaf Aslar A, Ergun H, Halil Elhan A, Memikoğlu O, Bulent Erkek A, Ayhan Kuzu M.

Dis Colon Rectum. 2011 Aug;54(8):923-9. doi: 10.1097/DCR.0b013e31821cc1f9. PMID: 21730779 [PubMed - indexed for MEDLINE]

Perianal abscess: a pilot study comparing packing with nonpacking of the abscess cavity. Tonkin DM, Murphy E, Brooke-Smith M, Hollington P, Rieger N, Hockley S, Richardson N, Wattchow DA. Dis Colon Rectum. 2004 Sep;47(9):1510-4. Epub 2004 Jul 8. PMID: 15486749 [PubMed - indexed for MEDLINE]

Perianal hidradenitis suppurativa. The Lahey Clinic experience. Wiltz O, Schoetz DJ Jr, Murray JJ, Roberts PL, Coller JA, Veidenheimer MC. Dis Colon Rectum. 1990 Sep;33(9):731-4. PMID: 2390907 [PubMed - indexed for MEDLINE]

[Experience on the treatment of acute anorectal abscess with primary fistulotomy]. Wu CL. Gaoxiong Yi Xue Ke Xue Za Zhi. 1990 May;6(5):218-23. Chinese. PMID: 2362300 [PubMed - indexed for MEDLINE]

The incidence of recurrent abscesses or fistula-in-ano following anorectal suppuration. Vasilevsky CA, Gordon PH. Dis Colon Rectum. 1984 Feb;27(2):126-30. PMID: 6697831 [PubMed - indexed for MEDLINE]

Management of perianal sepsis in a district general hospital. Fielding MA, Berry AR. J R Coll Surg Edinb. 1992 Aug;37(4):232-4. PMID: 1383516 [PubMed - indexed for MEDLINE]

COMPLICATIONS OF ACUTE APPENDICITIS AND OF THEIR TREATMENT Dr Brandon Jackson, Department of Surgery, Faculty of Health Sciences, University of Pretoria.

Appendicitis was first described in the 16th century as perityphlitis (inflammation of the connective tissue around the caecum)1. In 1886, Reginald H. Fitz describedthe pathogenesis starting with acute inflammation of the appendix to peritonitis and iliac-fossa abscess. Fitz also recommended surgical remedy for most cases2.In 1889, McBurney described the clinical findings. Appendicectomy is still the mainstay of treatment1.

Pathology and pathogenesis

• Appendix lumen obstruction leads to congestion within the appendix • Secretion of inflammatory exudate and mucous causes increase in luminal pressure • Obstruction of lymphatic drainage leads to further oedema, ulceration, bacterial growth and formation of pus leading to ischaemia of the appendix. • The loss of integrity leads to bacterial invasion of the submucosa and muscularis propria resulting in acute appendicitis. • On the rare occasion when the initial stages of infection resolves, the appendix distends with mucus resulting in a mucocele1.

Appendicitis complications • Gangrenous Appendicitis: Thrombosis of the appendiceal artery and veins leads to ischaemic necrosis3. • Perforation: The morbidity and mortality increase significantly following rupture of the appendix, with complication rates as high as 58 %5. A review of 653 cases of pathologically diagnosed appendicitis showed a perforation rate which is increased at both ends of the age spectrum. This is most likely due to delays in presentation and diagnosis4. • Peri-appendiceal abscess: The most frequent complication of perforation. The abscess remains localized if peri-appendicealfibrinous adhesions develop before rupture3. • Peritonitis: Bacterial peritonitis is due toperforation before formation of inflammatory adhesions3.A study of 2522 cases intraoperative cultures of peritoneal fluid showed no growth in 64% of normal cases, 65% with acute appendicitis and 24% with perforated appendicitis. Cases with positive cultures isolated most commonlyEscherichia coli followed by Enterococcus and other Streptococcus species. Less commonly encountered organisms cultured were Pseudomonas, Klebsiella, and Bacteroides species4.Refer to figure 1. • Bowel Obstruction: Mechanical obstruction, likely secondary to entrapment of the distal ileum in a peri-appendiceal inflammatory mass3. • Septic seeding of mesenteric vessels: Ascending infection along the draining mesenteric–portal venous system results in pylephlebitis, pylethrombosis, or hepatic abscess3. • Appendicitis and Pregnancy: About one in five patients present with complicated appendicitis and a perforation rate of 15-20% which is reportedly highest in the first and second trimesters. Appendicitis in pregnancy is associated with up to a 5% risk of fetal loss which increases to 20% if perforation occurs1. 93

Figure 1: Distribution of organisms isolated from peritoneal cultures stratified by diagnosis4.

Management of Appendicitis

A meta-analysis of post-intervention complications in suspected uncomplicated appendicitis was lower in patients who were managed with appendicectomy (0.8%) than in patients managed with antibiotic therapy (10%)6.

A meta-analysis of comparison of the management of complicated appendicitis showed that conservative management with or without Interval appendicectomy, is associated with a decreased complication and re-operation rate compared with appendicectomy. Conservative treatment is associated with less wound infections, abdominal/pelvic abscesses, and ileus/bowel obstructions7.

Timing of Appendicectomy

A prospective study of 723 patients (83% had Open appendectomy and 17% had Laparoscopic appendectomy) showed thatdelaying appendectomies by 12–24 h had no impact on the perforation rate, operative time, complication rate or length of hospital stay. Delaying appendectomy more than 24 h after presentation had a significantly increased complications rate (18.5 %). The number of gangrenous appendices was significantly higher and the histology showed a worse grade of inflammation5. Refer to Figure 2.

Figure 2: Comparison of the complication rate in the early appendectomy (EA)(< 12hrs from admission), early-delayed appendectomy (EDA)(12-24hrs from admission) and delayed

appendectomy (DA)(>24hrs after admission) groups5.

Interval Appendicectomy

Inflammation associated with abscess formation or phlegmon may complicate an immediate appendectomy, leading to injury of adjacent loops of small bowel12. Some authors prefer an immediate appendectomy and insist on a low morbidity rate, the reduction of the hospitalization stay, and also on the early diagnosis and treatment of unexpected pathologies13. Due to the associated morbidity some surgeons will treat this situation conservatively in the face of abscess or phlegmon and return 6-12 weeks later to perform an interval appendectomy.Interval appendicectomy is controversial as the risk of recurrent appendicitis is low compared to the risk of complications from interval appendectomy12.

Patients that undergo an interval appendicectomy, 16% will have a normal or obliterated appendix on pathologic evaluation and will likely not benefit from interval appendectomy. 84% of patients will have persistent acute appendicitis, chronic appendicitis, evidence of inflammatory bowel disease, or neoplasm identified, and likely benefit from surgical appendectomy. However, patients with appendicoliths are most likely to benefit from interval appendectomy as this becomes an environment for future infection12.

Laparoscopic versus Open Appendicectomy

A decreased incidence of wound infections has been considered to be a major advantage of laparoscopic appendectomy. Randomization resulted in 82 patients with open and 87 patients with laparoscopic appendectomy. 6% had wound infections after Laparoscopic appendicectomy—all of them at the umbilical incision—and 7% after Open appendicectomy8. Refer to Table 1.

Table 1:

However, a meta-analysis of all formally randomized prospective trials of Laparoscopic versus Open appendicectomy in adults showed the wound infection rate in the Laparoscopic appendicectomy is less than one half the rate in the Open appendicectomy group. The incidence of intra-abdominal abscess is higher in the Laparoscopic appendicectomy group, but this failed to reach statistical significance9.

The management of complicated appendicitis, i.e. gangrenous, perforated appendicitis and appendiceal abscess, remains controversial with regard to Laparoscopic or Open appendicectomy. There is also some concern related to higher technical demand, longer operative time, and reported higher incidence of intra-abdominal collections in Laparoscopic appendicectomy.A retrospective study was conducted between 1999-2004 to evaluate the feasibility, safety, and efficacy of Laparoscopic appendicectomy when compared with open appendectomy in patients with complicated appendicitis.Theincidence of intra-abdominal collection rates for patients who had Laparoscopic appendicectomy or Open appendicectomy, was 5.7% and 4.3%, respectively (p = 0.473). The conclusion was that Laparoscopic appendicectomy for complicated appendicitis is feasible and safe and has less risk of wound infection (p<0.001)10.Refer to Table 2.

Table 2: Laparoscopic (LA) Versus Open Appendectomy (OA) for complicated appendicectomy10

Drain vs. No drain

Post laparoscopic appendicectomyintra-abdominal abscess formation may be more frequent because of spillage within the abdominal cavity of infectious contents, promoted by the carbon dioxide pneumoperitoneum. Allenmann et al. looked prospectively at 320 consecutive patients that underwent laparoscopic appendectomy for complicated acute appendicitis and found a statistically significant lower overall complication rate in the no- drain group, compared to the drained group (7.7% vs. 18.5%, p=0.01), mainly due to low- grade complications. Abdominal wall abscesses were significantly more frequent in the drain group. Therefore the advantage of the laparoscopic over the open approach, i.e., the reduced wound infection rate, is eliminated by routinely inserted drains11.Refer to Figure 3.

Figure 3: Details of surgical complications and drains11

NOTES (natural orifice transluminal surgery)

NOTES procedures, especially transvaginal access, still remain controversial from patients’ and physicians’ point of view.

A prospective study was done on 13 patients that underwent transvaginal-hybrid NOTES appendectomy. One patient developed an intra-abdominal abscess (with a vaginal fungal infection) and another infected hematoma, both occurred after a perforated appendicitis. There is no impairment of sexual function for up to 2 years or child-delivery following this operative access. Intraoperative and early postoperative data seem comparable to that of Laparoscopic appendicectomy. NOTES also prevents abdominal wall trauma like trocar hernias. NOTES appendectomy is therefore an alternative to Laparoscopic appendicectomy14.

Summary of Post-operative complications

Complications may be classified as early and late based on their time of presentation postoperatively.

Early complications (within the first week postoperatively), the most common early complication following appendicectomy for perforated appendicitis is wound infection. Patients undergoing primary appendicectomy with antibiotic prophylaxis have a surgical wound infection rate of 2.8% compared with 11.8% without the use of antibiotic prophylaxis6. The most common causative organisms are Gram negative bacilli and anaerobes. Wound drainage may be indicated based on clinical findings and antibiotics given pre- and intraoperatively can reduce the rate of wound infection1.

Intra-abdominal abscessesare twice as likely to occur in gangrenous or perforated appendicitis and is responsible for the majority of reported deaths after Laparoscopicappendicectomy4. The most common sites for this include between loops of small bowel (interloop), pelvic, subphrenic and paracolic sites1. Postoperative ileus should 97

be managed conservatively by keeping the patient nil by mouth, IV fluids and the insertion of a nasogastric tube. Port site haematomafor laparoscopic appendicectomy can be avoided by removing ports under vision1.

Postoperative leak following appendectomy<48 hours the patient should be taken back to the exploration.Leaks that are suspected > 48 hours after a laparoscopic appendectomy, should be assessed in the context of the patient’s clinical status. If the patient is stable and does not show signs of diffuse peritonitis, a CT scan is recommended to assess the presence of intra-abdominal abscesses.

Late complications (more than 1 week post appendicectomy) include adhesional obstruction, faecal fistula, and incisional hernias. They are rare and may occur up to a few months to years after surgery and more frequently occur in females, diabetics and those with perforation or peritonitis at the time of surgery. Incisional hernias following the open technique occurs in less than 0.12% of patients1. Urinary tract disorders (retention and infection) accounted for 25% of all complications and is slightly more common in patients with perforated appendicitis. More than half of postoperative pneumoniasare associated with the presence of perforation4.

Miscellaneous complications encountered include pseudomembranous enterocolitis, pulmonary embolus, acute renal failure, myocardial infarction, deep venous thrombosis, and common iliac artery laceration secondary to laparoscopic trocar insertion4.

References

1. Chandrasekaran TV and Johnson N. Acute appendicitis. Surgery. 2014. 32 (8): 413- 417. 2. Berry J and MALT RA. Appendicitis near Its Centenary. Ann. Surg. 1984; 200 (5):567-576. 3. Leite NP, Pereira JM, Cunha R, Pinto P and Sirlin C. CT Evaluation of Appendicitis and Its Complications: Imaging Techniques and Key Diagnostic Findings. AJR. 2005; 185:406–417. 4. Hale DA, Molloy M, Pearl RH. F.A.C.S., David C. Schutt, M.D., and David P. Jaques. Appendectomy: A Contemporary Appraisal. ANNALS OF SURGERY. Vol. 225, No. 3, 252-261. 5. Giraudo G, Baracchi F, Pellegrino L, Dal Corso HM and Borghi F. Prompt or delayed appendectomy? Influence of timing of surgery for acute appendicitis. Surg Today. 2013; 43:392–396 6. Kirby A, Hobson RP, Burke D, Cleveland V, Ford G, and West RM. Appendicectomy for suspected uncomplicated appendicitis is associated with fewer complications than conservative antibiotic management: A meta-analysis of post-intervention complications. Journal of Infection. 2015. 70: 105-110. 7. Simillis C, Symeonides P, Shorthouse AJ and Tekkis PP. A meta-analysis comparing conservative treatment versus acute appendectomy for complicated appendicitis (abscess or phlegmon). Surgery 2010; 147: 818-29. 8. Klingler A, Henle KP, Beller S, Rechner J, Zerz A, Wetscher GJ, et al. Laparoscopic Appendectomy Does Not Change the Incidence of Postoperative Infectious Complications. Am J Surg. 1998; 175:232–235. 98

9. Golub R, Siddiqui F and Pohl D. Laparoscopic Versus Open Appendectomy: A Meta- analysis. Am Coll Surg 1998;186:545–553. 10. Yau KK, Siu WT, Tang CN, Cheung Yang GP, KaWah Li M. Laparoscopic Versus Open Appendectomy for Complicated Appendicitis. J Am Coll Surg 2007;205:60–65. 11. Allemann P, Probst H, Demartines N and Schäfer M. Prevention of infectious complications after laparoscopic appendectomy for complicated acute appendicitis— the role of routine abdominal drainage. Langenbecks Arch Surg (2011) 396:63–68. 12. Lugo JZ, Avgerinos DV, Lefkowitz AJ, Seigerman ME, Zahir IS and Lo AY. Can Interval Appendectomy be Justified Following Conservative Treatment of Perforated Acute Appendicitis? Journal of Surgical Research. 2010. 164: 91–94. 13. M. Martin, J. Lubrano, A. Azizi, B. Paquette, N. Badet and E. Delabrousse. Inflammatory appendix mass in patients with acute appendicitis: CT diagnosis and clinical relevance. Emerg Radiol (2015) 22: 7–12. 14. Knuth J, Heiss MM and Bulian DR. Transvaginal hybrid-NOTES appendectomy in routine clinical use: prospective analysis of 13 cases and description of the procedure.SurgEndosc. 2014; 28:2661–2665

COMPLICATIONS OF TOTAL THYROIDECTOMY Prof LM Ntlhe, Department of Surgery, University of Pretoria and Steve Biko Academic Hospital

INTRODUCTION

Palpable thyroid nodules occur in 3- 7% of the population and ultrasound shows that the actual prevalence is up to 50%.

The number of thyroidectomies in the USA IS 118,000 – 166,000 per annum, having trebled in the last three decades.

The USAgency for Healthcare Research and Quality Statistics (AHRQ) conclude that the incidence of thyroidectomies in the US to be 37.4/ 100,000 population.

Indications for total thyroidectomy (TT) are Cancer, Pressure symptoms, Cosmesis and fear of malignancy

COMPLICATIONS ASSOCIATED WITH TT :

1) Recurrent (RLN) and Superior Laryngeal Nerve injury (SLN)

2) Hypocalcaemia due to Parathyroid Gland (PG) injury

3) Haemorrhage

4) Endotracheal Intubation and Extubation Risks

5) Other rare complications:

-Thyroid Storm

- Tracheomalacia

- Pneumothorax

- Thoracic duct / Right Lymphatic trunks injury and chyle leak

- Brachial plexus injury

- Oesophageal ,Laryngeal and tracheal injury

- Cervical Sympathetic damage…Horner’s Syndrome

-Phrenic nerve injury

7) Recurrence

SURGICAL Techniques:

a) Standard Open method b) Minimally Invasive Video- Assisted Thyroidectomy (MIVAT)

PRE- OPERATIVE ASSESSMENT

-A thorough History and Physical examination to evaluate and manage any comorbidities

- Thyroid assessment including its functional status, patients should be rendered euthyroid

100

-ENT assessment including Voice evaluation, may need baseline audio-recording when indicted and laryngoscopy.

- FNA Biopsy

-Imaging:

CXRay, Inlet Xray; CT or MRI when indicated.

INTRA- OPERATIVE MANAGEMENT

Anaesthetic:

Collaboration with the anaesthetist is mandatory

Need for advanced intubation techniques

Surgeon may have to perform an emergency tracheostomy

Valsalva maneuver at TT completion to assess bleeding

Extubation in OT or in ICU or High care.

Surgical technique:

The surgical anatomy is of paramount importance.

Relationships of the to be removed gland to the recurrent laryngeal nerves (RLNs), superior laryngeal nerves (SLN) (Internal and External branches: - IB-SLN and EB-SLN), parathyroid glands (PGs) superior and inferior pairs, carotid sheath,laryngo-tracheal axis, oesophagus and other structures.

1) RECURRENT LARYNGEAL NERVE:

On the right side it recurs around the 4th aortic arch (Subclavian artery). It is 5-6cm long reaching the Cricothyroid joint.

On the left side it is 12cm long reaching the cricothyroid joint.

Both nerves ascend to the tracheo-oesophageal groove. At the ligament of Berry(posterior position) the nerve divides into smaller sensory branches and the main motor branch which enters the larynx below the inferior constrictor muscle.

The RLNs are supplied by vasanervora from the Inferior Thyroid Artery (ITA) therefore excessive stretching may render them ischaemic.

ANATOMICAL VARIATIONS of the RLNs:

1) Non- RLN: Emerges at a right angle from the cervical vagus, often associated with dysphagia lusoria on the right side, incidence ( 0.3-1.6%)and 0.04% on the left side. 2) Variation in branching; extralaryngeal branching with the main motor branch at risk (motor to 4 intrinsic muscles) and sensory to glottic mucosa 3) Variable relation to ITA & Berry ligament: a) May take a medial course to ligament b) May penetrate the ligament especially the motor fibers and thus endangered at the end of TT

101

Soustelle’s Classifiction of Non-RLN:

Type 1: arise from the cervical vagus at 90° and enters the larynx at the upper pole with the Superior Thyroid Artery (STA) and vein.

Type 2a: Arize near origin of STA and enters the larynx above the STA

Type 2b: Arize near the origin of the ITA and enters the larynx below the ITA

Danger in type 1…mobilizing the superior pole

Danger in type2….nerve may be mistaken for ITA and ligated.

Pre-Op CT scan: Dysphagia Luzoria picture alerts the surgeon US scan : Absence of horizontal Υ figure of the brachiocephalic artery predictor of a Non- RLN.

Intra-operative Nerve Monitoring (IONM) is valuable in repeat surgery or irradiated necks.

There is a lack of high level evidence showing the effect of IONM, it also does not monitor sensory function.

Some use methylene blue spray to stain the RLNs and PGs.

NB: Active search and visualization is the cornerstone of RLN protection.

Simon’s triangle: RLN is usually found in this space

-oesophagus medially

-carotid artery laterally

-ITA superiorlly

RLN lesions

Transient partial – segmental demyelination or focal conduction block

Transient or Permanent total RLN – severe myelin sheath and axonal damage and neural degeneration

Transient palsies are due to Neuropraxia or axonotmesis depending on:

a. Local myelin damage by: oedema. Poor perfusion or blood clot b. Loss of axon continuity

Clinical Features

• Hoarseness in unilateral lesions • Acute stridor and airway obstruction with bilateral lesions • Dysphagia due to injury to posterior branches of RLN to cricopharyngeus muscle and oesophagus, esp for liquids 102

• Professional singers and public speakers suffer voice incapacity • 33% are asymptomatic

Treatment – difficult

• Should be symptom focused

Once diagnosis is made – management belongs to the domain of the ENT Surgeon therefore refer early (multidisciplinary team including voice specialists)

Management

Bilateral cord paralysis

- Both the intrinsic muscles are paralysed and both vocal cords adopt a median or paramedian position due to the unopposed actions of cricothyroid muscle

Clinical features:

- Acute dyspnoea at extubation - Voice change

Treatment:

1) Re- initubate and maintain ventilation - Some people use corticosteriod therapy to reduce laryngeal oedema - 20-60 mg solumedrol IVI over 30 minutes – 8 hourly - Dexamethasone 4-10 mg /day - Add broad spectrum antibiotic and PPI cover 2) Persistent paralysis – tracheostomy Recovery is unusual in these cases – may take upto 12 months 3) Surgical treatment Lateralization of the cords by - Arytenoidectomy with posterior cord resection to restore air passage. Endoscopically or open surgery - Implantation of sternohyoid - Thyroplasty

Disadvantage: voice quality is poor, transient aspiration and dysphagia but patients tend to tolerate this trade off.

Unilateral RLN paralysis

All intrinsic muscles except the cricothyroid are paralysed on that side

Asymptomatic in 33% of patients

Voice change which improves with speech therapy

Evaluate the patients’ tolerance, QOL, phonation and respiratory function

Surgical Corrective Procedures

1) Medialization of the vocal cord by intra-cordal antologous material injection (fat) via endoscopic or transcutaneously route 2) Thyroplasty – implantation via thyrotomy of various materials into the paralysed cord 3) Traction suture – Adduction of the arytenoids muscle 103

4) Repair of RLN by primary suture with 6 – 0 prolene or nerve graft

2) SUPERIOR LARYNGEAL NERVE (SLN)

Galli Curci nerve – named after the Italian opera singer whose career plummeted post thyroidectomy and “it was ultimately said to be due to physiological aging of the singer”.

The SLN originates just below the dorsal ganglion of the vagus nerve below the jugular foramen.

Divides into the Internal Branch (IBSL) which pierces the thyrohyoid membrane accompanied by the STA provides sensory function to the laryngeal mucosa and the EB- SLN about 1.5 cm from its origin.

EB-SLN nerve is 0.8 m wide and 8-9 cm long. It courses antero-inferiorly along the inferior constrictor muscle with branches of the STA, it then curves anteriorly and medially in the Space of Reeve: Steno thyroid muscle insertion superiorly, inferior constrictor and cricothyroid muscle medially and the superior pole of the thyroid inferio- laterally.

Risk of injury is significant when dissecting the superior thyroid pole vessels.

Cernea’s classification of the EB-SLN in relation to the distance between intersection of EB-SLN and STA and the superior pole of the thyroid gland.

Type 1 (60%) – crosses STA 1cm above superior pole to gland.

Type 2 (a) (17%) – crosses STA < 1cm above superior pole of gland

Type 2 (b) (20%) – crosses STA below the superior pole of gland

Type Nί (3%) – EB-SLN not identified :– sub fascial; intra muscular route

Both type 2a and 2b are usually at high risk.

EB-SLN supplies motor to the cricothyroid muscle – tilts thyroid cartilage and tenses the vocal cords by modifying the distance between the cricoid and thyroid cartilages

Vocal cord tension and thickness affects the frequency of vibration and therefore affects the characterization timber of one’s voice.

Injury rates: 0-58% (no protocols available to guide diagnosis and management)

Injury to EB-SLN results in weakness of the cricothyroid muscle

• Decreased voice quality • Decreased voice projection • Decrease in pitch

Risk of injury at superior pole

Landmark – nerve lies on the inferior constrictor, therefore one may have to divide the sternothyroid muscle and elevate it, especially for large goiters, to make superior pole dissection easier in order that the SLN could be identified.

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Gentle caudo-lateral traction of thyroid gland gives good exposure of the superior pole vascular pedicle. Avoid excessive traction and diathermy

Identification of the SLN is by gentle blunt (peanut) dissection of the superior pole from the medial aspect in the avascular space between superior pole and cricothyroid muscle.

Very few (3-10%) superior laryngeal nerves are actually visualized at surgery

Intra-op aids:

- Endoscopic visualization - Intra-op neuro monitoring

Injury to the SLN:

Voice fatique, reduction in high pitch voice, dysphagia, dyspnoea, worse for singers.

Post op aids: Video stroboscopy – muscosal waves

Electromyography–cricothyroid action potentials

Uncomfortable to patients

Unilateral, combined RLN and SLN

All the muscles on one side are paralysed. Vocal cord is in cadaveric position, 3.5 mm from the midline.

Clinical features:

- Hoarseness of voice - Aspiration through ineffective glottis - Ineffective cough

Treatment:

- Speech therapy. (Commonly healthy opposite cord moves to the opposite side of the midline so as to compensate for the paralysis of the opposite side) - Injection of Teflon to the paralysed cord - Muscle or cartilage implant into the paralysed cord - Arthrodesis of cricoarytenoid joint

3) HYPOCALCAEMIA:

Definition

- Total serum calcium < 2mm/L (< 8.0 mg/dl) Normal range (8.5-10.2mg/dl) - Ionized calcium < 1.1 mm/L (< 0.275 mg/dl) Normal range (4.5-5mg/dl)

Incidence – 2 – 83% depending on definition

- Some include only symptomatic patients, others do not in management decision

Long term low calcium occurs in <3% 105

Cause – decreased PTH secretion resulting in low calcium levels and usually associated with increased phosphate levels.

Risk of post operative hypocalcaemia – transient or permanent is due to:

1) Venous flow from the superior parathyroid gland is through the thyroid gland therefore reduction in circulating PTH 2) Sub capsular or intra-thyroid parathyroid glands especially inferior glands results in 6- 21% accidental parathyroidectomy and transient hypocalcimia – 50% cases 3) Massive goiter, Grave Disease, Thyroid Ca with lymph node dissection risks removal of lower PTGs 4) Devascularization during surgery especially with repeat thyroidectomy

NB – post operative PTH level is a better predictor of hypocalcaemia compared to a single value of low ionized serum calcium and Wand et al propose no supplementation if PTH level ≥5 pg/ml

- Measure PTH 6 hours post op (Grodski Australian meta-analysis) - Noordzi showed that a decrease of > 65% basal PTH level at 6 hours post op predicts hypocalcaemia (sensitivity 96.4 %, specificity 91.4%)

Visualization of at least 2 glands is enough at operation

Careful protection of PTG blood supply

Devascularized parathyroid glands should be auto-transplanted into sternocleiodomastoid or forearm muscle.

Pre-op detection of Vit D (25OH–Vit D3) below 20ng/ml. Treat with 100, 000U of oral cholecalciferol

Management of Hypoparathyroidism:

Diagnosis: Low PTH and decreased calcium ideally 6 hours post op

Treatment combined calcium and Vit D therapy

Symptomatic patients – especially with tetany

Neuromuscular excitability, parasthesia, carpo-pedal spasm.

Calcium <1.75 mM/l (<7 mg/dl) with Tetany etc., with a risk of cardiac decompensation

1) IVI – calcium Gluconate (1-2 ampoules of 10% solution for 24-48 hours plus, 2) Oral calcium (3g) – carbonate - Citrate - Chloride plus, 3) Dehydrocholecalciferol 2μg plus, 4) Magnesium 1-2g if there is hypomagnesaemia

Calcium gluconate IVI: 1 ampoule IV bolus followed by infusion of 1-3mg in 500ml DW over 12 hours for 10 days (to avoid arrhythmic CCF) or until symptoms abate.

Long term treatment dose caution: avoid hypercalciurea and renal stones.

Therefore Aim:

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1) Calcium and Phosphate product of 4.44 mM/L 2) 24 hour urine calcium < 300mg (7.5 mM/L)

Parathyroid gland recovery may take months to recover and if so start to wean the patient.

4) POST OPERATIVE HAEMORRHAGE

Incidence: 0-6.5%

Causes: Slipped ligature, parenchymal bleed etc.

Clinical Presentation:

- Overt bleed - Haematoma – compressive/non-compressive with respiratory distress - Pain - Can occur beyond 6 hours post op – therefore monitoring in the ward for 24 hours - Respiratory compromise

Leyre et al., 70 patients of 6744 did bleed and 10% after 48 hours

- NB anticoagulant and antiplatelet therapy do not seem to be risk factors as long as the surgery is meticulous. - Haemorrhage due to IJV injury may also cause air-metabolism

Management

1) Prevention - Control hyperthyroidism - Intra operative haemostasis - Valsalva maneuvre at completion of TT 2) Treatment - Urgent re-exploration, evacuation and drain - Ligate bleeders (rarely found) 5) OTHER COMPLICATIONS 1) Thyroid storm – rare Mx - pre-op care is excellent these days 2) Tracheomalacia – rare, large goiter, Mx – Tracheopexy - Silastic rings 3) Horners syndrome – rare, ptosis, enophthalmic

Rx – Conservative

- Cosmetic surgical correction

Infection

Pneumothorax

Thoracic duct injury and chyle leak

Branchial Plexus injury

Oesophagus - repair and adequate drainage

- Antibiotics 107

REFERENCES

1. N Christian, M Mathonet. Complication after total thyroidectomy; Review Journal of visceral surgery 150, 249-256 2013/04/03

2. S S Chandrasekha, G W Randolh, MD Seidman et al Clinical Practice Guideline; Improving Veric Outcomes after Thyroid Surgery; American Academy of Otolaryngology – Head and Neck surgery foundation 2013 http;://otojournal.org

3. Amy Y Chen, VJ Bernet, SE Carty et al; American Thyroid Association Statement on Optimal Surgical Management of Goiter

4. L Rosato, N Avenia, P Bernate et al. Complications of Thyroid Surgery; Analysis of a Multicentric study on 14 934 Patients Operated on in Italy over 5 years. World J Surg 28(3) 271-276 3/2004

5. CJ Kerawala, M Heliotos. Review: Prevention of Complications following Neck dissection: H & N Oncology 1(35) 10/2009

6. E. Varaldo, GL Ansalalo, M mascherini et al. Neurological Complications in Thyroid Surgery; A Surgical Point of View on Laringeal nerves. Frontiers in Endocrinology: 5: 108: 1-10 7/2014

7. T Berri, R Houari. Complications of Thyroidectomy for large goiter: case report Pan African Medical Journal 11/12/2013

8. S Saris, E Ayson, YE Ersoy et al. Safe Thyroidectomy with intra operative methylene blue spraying: Thyroid research: 5:15 2012

9. B H-H Lang PC –Yih, C-Y Lo. A review of risk factors and timing for post op haematoma after thyroidectomy: is outpatient thyroidectomy really safe. WJS 2012 Oct 36(10) 2497 – 2502.

10. W.S. Duke, JR White, JL Waller et al. Six-year experience with endoscopic thyroidectomy outcomes and safety profile. Annals of Otology, Rhinology and Laryngology.

11. X-D Chen, B Peng, ri Xiang et al. Endoscopic thyrodectomy: an evidence based research on feasibility, safety and clinical effectiveness. Chinese medical journal 321(20) : 2088-94 10/2008.

12. Trends in Robotic Thyroid Surgery in the United States from 2009 through 2013. A.M Hinson, E. Kandil, S.O’ Brien et al. Thyroid Vol 25(8), 919-926. 2015

13. Sriram Bhat M. Recurrent laryngeal nerve palsy: in 3rd Ed, SRB’s Manual of Surgery. JP Brothers Medical Publishers. pgs 441-443. 2009

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Abstract

Diseases of the thyroid gland are common and usually present as goiter. Rarely, patients present due to abnormal function which may not necessarily be associated with enlargement. Majority of thyroid diseases do not require involvement of a surgeon. However surgeons get involved when there is hyperthyroidism, need to exclude thyroid malignancy and for management of compression symptoms. Crisis associated with management may result from consequences of extreme derangement of thyroid function, mass effect or complications of treatment such as thyroidectomy. Thyrotoxicosis crisis is extremely rare. Crisis situations which a surgeon is likely to encounter are airway obstruction, bleeding, bilateral recurrent laryngeal nerve damage and hypocalcaemia.

Introduction

Goiter is common but involvement by a surgeon is necessary only if there is abnormal thyroid function, fear of malignancy, compression symptoms, retrosternal extension and rarely for cosmesis. Irrespective of how a patient would have presented clinical evaluation is standardized. Similarly, the first step in diagnostic investigation is determination of serum thyroid stimulating hormone level. Probability of thyroid malignancy is based on a combination of personal, family and environmental risk assessment on history. Compression symptoms are likely in patients who have large goiter, asymmetric goiter with tracheal shift and goiter extending retrosternally. Diagnosis of retrosternal extension is clinical. Chest and neck CT scan is mandatory for patients who have retrosternal extension to enable grading and thyroid malignancy with extensive lymphadenopathy.

Thyrotoxic crisis

A surgeon is likely to encounter hyperthyroidism than hypothyroidism and may therefore occasionally have to deal with cases of thyrotoxic crisis or so called thyroid storm (Kearney and Dang, 2007; Ross, 2011; Jit et al, 2015). Causes of hyperthyroidism which can lead to thyrotoxic crisis are Graves’ disease, toxic multinodular goiter and toxic adenoma. It is however relatively more likely in Graves’ disease generally and in elderly, patients with underlying cardiovascular disease or have severe hyperthyroidism i.e. hyperthyroidism with deranged cardiac function or marked elevation of thyroid hormones (T4 or T3 more than twice above the upper limit of normal range) irrespective of the underlying cause.

Any stress can precipitate thyrotoxicosis crisis. Such stress include infections, surgical procedures (not necessarily thyroidectomy), following I-131 ablation. Almost every organ- system in the body is affected during a thyrotoxic crisis and the manifestations are mainly due to sympathetic hyperactivity. The following systems are most frequently involved: central nervous system, cardiovascular system and gastrointestinal system. Common manifestations include deranged level of consciousness, cardiac arrhythmias, cardiac failure, malignant hyperthermia, etc. Rarely, apathetic thyrotoxic storm may occur in elderly patients.

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As it was mentioned previously thyrotoxic crisis is unusual in patients diagnosed with hyperthyroidism who are adequately prepared medically for thyroidectomy or radioablation. Because of a relatively long half-life of thyroid hormones (especially T4), it is advisable to extend treatment with antithyroid drugs beyond the day of definitive treatment to prevent a crisis which may be induced by a surge of hormones released during surgery or radiation driven destruction of the gland. Although pre-procedure preparation with beta blocker alone may be adequate for patients who have mild hyperthyroidism the same is not true for moderate and severe thyrotoxicosis. Clinical and biochemical euthyroidism has to be secured before intervention such as thyroidectomy is implemented. Furthermore, perhaps the major preventative strategy if for surgeons to stop doing thyroidectomy for hyperthyroidism except in less than 1% of patients presenting with hyperthyroidism irrespective of the cause.

Patients in thyrotoxic crisis should be treated in ICU and treatment package include general supportive measures such as fluid therapy and lowering of body temperature, strategies to blunt sympathetic over activity such as using intravenous beta blockage, blocking peripheral conversion of T4 to T3 (propranolol, corticosteroids and propylthiouracil), blunting/stabilizing of receptors (corticosteroids), blocking hormogenesis (antithyroid drugs and iodine) and blocking the release of pre-formed thyroid hormone (iodine containing intravenous contrast or lithium). Diuretics such as furosemide are contraindicated. It is also important to treat the precipitating cause. Predicted mortality in patients who has thyrotoxicosis crisis is 30%.

Myxoedema coma

Myxoedema coma following thyroidectomy is rare. Elderly patients are most at risk (Bajwa and Jidal, 2015). It is only expected after more than 4-6 months following total thyroidectomy if a patient is not given replacement therapy. However hypothyroidism leading to myxedema coma may occur even after subtotal thyroidectomy if the remaining thyroid tissue is functionally insufficient such as in MNG or the procedure was done for Graves’ disease and a patient has high levels of destructive autoantibodies.

With adequate dosing and attention to pharmacodynamics of thyroxine severe hypothyroidism should not occur while a patient is on treatment. Acute hypothyroidism may be induced by a critical illness in patients who seemingly were in a euthyroid state. Predominant manifestations involve same organ-systems i.e. central nervous system, cardiovascular and gastrointestinal systems which are affected a thyrotoxic crisis. Recombinant TSH or T3 can be used to shorten the duration a patient is left off thyroid hormone replacement and suppression in preparation for whole body scan during follow up of differentiated cancer of follicular cell origin following total thyroidectomy.

A relatively early consent following treatment of hyperthyroidism is potential of worsening of Graves’ ophthalmopathy if a patient who has severe eye-disease is allowed to become hypothyroid. Treatment of myxedema is mainly supportive and background adrenal insufficiency should always be suspected. Therefore thyroid hormone replacement should be preceded by infusion of glucocorticoids. Precipitating cause must also be sought and managed.

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Airway obstruction/compromise

Airway challenges may occur pre-, intra- or post-operatively. Actually, acute airway obstruction might have been the indication for emergency thyroidectomy. Patients at risk of airway obstruction include individuals who have large nodular goiter and goiter with retrosternal extension (Agarwal et al, 2007). Difficult airway intubation is to be expected. Pre- operative CT scan should be done routinely. Consulting a team of anesthetists and ensuring that resources necessary for management of difficult airway in theatre is advisable. Invariably it usually end up as an anti-climax.

Post-operative causes of airway compromise include bilateral recurrent laryngeal nerve damage, tracheomalacia and haematoma. The risk for bilateral recurrent laryngeal nerve damage is higher during thyroidectomy for large nodular goiter, retrosternal goiter and malignant goiter associated with extensive lymph node enlargement as the course of the nerve might have been distorted and in re-do thyroid surgery. Unilateral nerve damage should always be assumed in patients who have had prior thyroid operation even if the voice is normal as the contralateral vocal cord could have undergone compensatory hypertrophy. Routine identification of the RLN throughout its course including of its branches is mandatory. Nerve monitoring is not helpful. Tracheostomy is absolutely necessary in patients who have suffered bilateral RLN damage.

Tracheomalacia is likely in patients who have huge goiter (Agarwal et al, 2007). Key treatment options include leaving a patient intubated (endotracheal tube) for 3-5 days or prophylactic tracheostomy. Strategies to prevent peri-operative bleeding following thyroidectomy include measures to reduce vascularity in thyrotoxic goiter (beta blocker therapy and iodine), meticulous dissection, ligation in continuity of inferior thyroid artery and using drains for complicated thyroidectomy or if thyroidectomy leaves a large potential space. Options for treatment of airway obstruction due to a haematoma include removal of sutures, re-operation or aspiration. Prophylactic drains placed during the operation are useless as the drainage amount often does not correlate with symptoms.

Hypocalcaemic crisis

Hypocalcaemia following thyroidectomy may be due to “hungry bone syndrome” or hypoparathyroidism. The hungry bone syndrome is due increased oestoclastic activity in patients with hyperthyroidism whereas hypoparathyroidism is mostly due to devascularization of parathyroid glands (Ciftci et al). Only in rare occasions are all parathyroid glands are removed. Preventive strategies include high index of suspicion, meticulous dissection, ligation of branches of the inferior thyroid artery on the gland, appropriate selection of energy device, avoiding of energy device when dissecting within 3mm of parathyroid glands, intra-operative intact parathyroid hormone and parathyroid gland auto-transplantation.

Conclusion

Severe complication following thyroid procedures include bleeding, airway obstruction/compromise resulting from bilateral RLN damage, tracheomlacia or haematoma, hypocalcaemia and extreme hypo- or hyperfunction. Crisis resulting from hypo-or hyperfunction are extremely rare and elderly individuals are most at risk. 111

References

1. Suslu N, Vural S, Oncel M, et al. Is the insertion of drains after uncomplicated thyroid surgery always necessary? Surgery Today 2006; 36: 215-218. 2. Nawrot I, Pragacz A, Pragacz K, et al. Total thyroidectomy is associated with increased prevalence of permanent hypoparathyroidism. Medical Science Monitor 2014; 20: 1675-1681. 3. Dionigi G, Boni L, Rausei S, et al. The safety of energy-based devices in open thyroidectomy: a prospective, randomized study comparing the LigaSureTM (LF1212) and Harmonic® FOCUS. Langenbecks Archives of Surgery 2012; 397: 817-823. 4. Ciftci F, Sakalli E, Abdurrahman I, et al. Parathyroid function following total thyroidectomy using energy devices. European Archives of Otorhinolaryngology DOI 10.1007/s00405-015-3704-8. 5. Ross DS. Radioiodine therapy for hyperthyroidism. The New England Journal of Medicine 2011; 364 (6): 542-550. 6. Bahn RS, Burch HB, Cooper DS, et al. Hyperthyroidism and other causes of thyrotoxicosis: management guidelines of the American Thyroid Association and American Association of Clinical Endocrinologists. Endocrine Practice 2011; 17(2): 456-520. 7. Agarwal A, Mishra AK, Gupta SK, et al. High incidence of tracheomalacia in longstanding goiters: experience from an endemic goiter region. World Journal of Surgery 2007; 31: 832-837. 8. Bajwa SJS and Jindal R. Endocrine emergencies in critically ill patients: challenges in diagnosis and management. Indian Journal of Endocrinology and Metabolism 2012; 16: 722-727. 9. Kearney T and Dang C. Diabetic and endocrine emergencies. Postgraduate Medicine 2007; 83: 79-86.

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MANAGEMENT OF COMPLICATIONS OF PAROTIDECTOMY Dr J K Jekel – Dept surgery University of Pretoria

The intimate relationship of the parotid gland and the facial nerve dictates that the facial nerve continuity be sacrificed occasionally for certain neoplastic lesions. This devastating insult to emotional expression is never entirely overcome after the facial nerve is transected. Although patients are told that facial paralysis will follow such operations, it is difficult to communicate to them the full impact of facial paralysis.

Parotid surgery is mostly undertaken in an attempt to remove benign tumours and thus complications should be minimized at all costs.

When the surgery is done to remove malignant tumours the histology should be known and the extent of the tumour evaluated before any attempt at removing the tumour is undertaken. This is important as the possibility of any complication can be pre-empted and fully discussed with the patient prior to the surgery. This is especially important if the facial nerve is possibly involved and decisions about sacrificing the nerve have to be made. Pre- operative discussions are a key factor in the patients understanding and acceptance of the surgical treatment.

Salivary complications of parotid surgery must also be discussed preoperatively as some patients will have decreased saliva production.

Cosmetic deformities of the face – especially if extensive surgery combined with mandibulectomy and neck dissections are undertaken can be expected. If the patient is to receive post-operative radiotherapy these deformities can be extensive.

The complications of parotid surgery will be divided into:

1. Local 2. Nerve damage 3. Salivary 4. Frey`s syndrome 5. Local cosmetic effects

Local complications

The local complications mostly consist of wound complications and must be treated if and when they occur. The best treatment of local complications is prevention and preoperative planning should prevent most complications.

1. Wound infection occurs in patients where infective conditions are associated with the indication for surgical intervention. These should be treated pre operatively with antibiotics or with antibiotic prophylaxis. Leakage of saliva into the wound causes severe septic complications and this can be prevented by proper drainage with suction drains. 113

2. Wound breakdown can be disastrous as this will usually expose the facial nerve and can cause damage to the nerve. If the tumour is close to the skin or the skin flaps are large with tedious blood supply it might be wise to use flaps ( rotation or free tissue transfer ) in an attempt to close the surgical defect. The skin must never be sutured under tension as this compromises blood supply to the skin flap and will lead to skin necrosis. Skin grafts are not indicated to cover the facial nerve.

3. Salivary fistulas occur in some cases – especially if a large portion of the parotid remains after the surgery. This can be prevented by removing most, if not all of the parotid tissue. To remove the deep lobe does however increase the possibility of nerve damage dramatically. Division and ligation of the ducts as they are encountered during the surgery as well as proper suction drainage decrease the possibility of fistulation. The treatment of fistulas by surgery is difficult and nerve damage as complication is very high. A short course of superficial radiotherapy with electron radiation usually stops saliva production and thus solves the problem

Nerve complications

The most devastating aspect of salivary gland surgery is certainly Facial nerve damage. Other nerves can however be damaged and this must be discussed pre operatively

1. Greater Auricular nerve. The greater auricular nerve is the sensory nerve to the ear and lateral part of the face. It exits behind sternocleidomastoid muscle and has a superficial course to the ear. It`s branches are frequently damaged as the skin flaps are lifted. Most of the branches run through the parotid substance but can be dissected out if the nerve is not close to the tumour.

2. Facial nerve damage. The course of the facial nerve through the substance of the parotid makes facial nerve damage an ever possible complication. Exploration of the main trunk with visualisation of the facial nerve and dissection on the plane of the nerve is the only way to prevent nerve damage. Nerve stimulators may be of value to detect the nerve. If the main trunk cannot be identified it is essential that the distal branches be dissected out and the nerve followed back to the main trunk.

A) If a planned resection of the nerve is done immediate reconstruction must be attempted. The surreal nerve is usually harvested from the leg and used as a cable graft

B) Nerve transposition can be attempted but should be used only if cable grafts are not possible. Hypoglossal-Facial anastomosis is the most successful of these anastomoses. Other nerves used include spinal accessory and phrenic nerve but these cause more disability than the Hypoglossal.

C) Facial reanimation by muscle transfer is used widely to attempt to minimize complications to the eye and prevent drooling. This should only be attempted if nerve

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reconstruction cannot be done or has failed. The muscle used most commonly and successfully is the Temporalis muscle. The Masseter has also been used.

D) Lateral Tarsorrhaphy is widely used to help protect the eye and prevent corneal ulceration.

The lateral parts of the upper and lower eyelids are sutured together after the skin has been denuded in an attempt to prevent ectropion and make closure of the eyes easier. The use of Gold weights in the upper eyelid was used but this is expensive and not used any more.

Salivary complications

Parotidectomy done for benign disease usually does not lead to a dry mouth as the other salivary glands function normally. Elderly patients do however frequently complain of dry mouth after parotid surgery. If radiation is planned as part of the treatment this aggravates Xerostomia. The use of newer radiotherapy modalities like IMRT can decrease xerostomia.

There is no treatment for xerostomia but these patients must be encouraged to drink water frequently and the use of chewing gums may help. Transient loss of taste is associated with xerostomia but this can be permanent.

Frey`s Syndrome or Gustatory sweating.

This is extremely common after parotid surgery and is characterized by flushing and sweating on the ipsilateral side of the face – especially during eating. The pathophysiology is the misdirected regeneration of sympathetic and parasympathetic fibres to the cholinergic receptors of the skins sweat glands. The treatment is directed to blocking the abnormal pathway.

Surgical procedures include resection of the nerve pathway, resection of the skin with grafting of the defect or destruction of the nerve fibres by alcohol injection.

The best treatment currently is injection of Botox.

Local cosmetic effects.

Most patients will accept a cutaneous concavity in the parotid fossa but in certain individuals the defect is less acceptable. If radiotherapy is not part of the treatment the surrounding skin and hair are normal and the defect can easily be hidden. Radiotherapy does however also make free grafts of skin and muscle difficult and most reconstructions must be done after radiotherapy effects have subsided.

The effect of radiotherapy

Radiotherapy is frequently used as adjuvant treatment in the management of malignant parotid tumours.

As discussed above this usually aggravates the complications encountered during parotid surgery. If radiation is planned the decision is usually made pre operatively and the surgery and reconstruction modified to minimize these effects.

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It is also important to look at oral hygiene and to extract teeth if necessary in order to prevent the problems associated with loss of salivary production and osteoradionecrosis.

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FAILURE OF BREAST RECONSTRUCTION AFTER BREAST CANCER SURGERY Dr S. Sehlale, Department Plastic Surgery

There is increased demand for post mastectomy breast reconstruction but the reconstruction options are rapidly evolving

The choice of reconstructive options is dependent on:

PATIENT FACTORS

 Lifestyle of the patient/patient’s wishes  Desire to have babies  Body habitus  Down time of procedure  Risk factors  Cancer prognosis

BREAST FACTORS

 Type of mastectomy +axillary procedure  DXT  Failed reconstruction  Timing of reconstruction  Status of opposite breast

GAOLS OF RECONSTRUCTION:

1. Volume (size of projection) 2. Envelope (shape & position) 3. Symmetry with contralateral breast 4. NAC

TECHNIQUES OF RECONSTRUCTION

 Alloplastic (Expander/implant)  Alloplastic & Autologous (flap & implant)  Autologous (flaps)

RECONSTRUCTIVE FAILURE – FAILURE TO ATTAIN RECONSTRUCTIVE GOALS

 Technical failure  Procedural complications  Unsatisfactory results

RECONSTRUCTIVE OUTCOME ANALYSIS

1. Complications Revision after prosthetic reconstruction is generally higher than for autologous. 2. Lower revision rates for autologous reconstruction - Lower overall major complications. - Better aesthetic outcome. - Long lasting acceptable results.

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CONCLUSION

“It is important to have an open mind and to rethink the treatment strategy … If the situation calls for a change in strategy and if the surgeon is flexible enough to pursue a new course, the reward will often be vastly improved result and a satisfied patient” Kroll & Freeman.

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COMPLICATIONS OF CAROTID STENOSIS SURGERY T.V. Mulaudzi, Vascular Surgeon

Introduction

The improvements in medical and surgical management in carotid artery stenosis have led to the steady decline in morbidity and mortality from ischemic stroke in the past several decades. However, this has not translated to a decline in the incidence of ischemic stroke1. Stroke is a truly debilitating condition and impacts significantly on the patient’s wellbeing, the family structure and is a burden on the social and healthcare systems. The role of surgical intervention on extra cranial carotid artery disease has had a telling effect on improving the outcomes of patients with atherosclerotic carotid artery disease.

Atherosclerotic disease of the carotid artery is seen to be a result of intimal injury followed by a process of inflammation, smooth muscle proliferation finally followed by calcium deposition. The resultant stenosis causes changes in flow and induces the phenomenon of flow separation. Furthermore, and probably more importantly, the process leads to plaque rapture, haemorrhage into the lesion and thrombotic events which subsequently may cause embolization to the cerebral circulation. Currently there is ongoing debate concerning the management option for carotid stenosis. Management of high grade stenosis in asymptomatic patients was until recently considered appropriate with pendulum swinging toward medical treatment for all asymptomatic patients without clear unstable plaque characteristics. Intervention is clearly indicated in the symptomatic patients with appropriate stenosis grades and in these patients surgical intervention in form of carotid endarterectomy is the procedure of choice. The debate concerning the management options is beyond the scope of this article, however, and this article will focus on the complications associated with carotid endarterectomy surgery.

Patients tolerate an uneventful carotid endarterectomy very well and hospital care does not have to continue beyond a 48 hours. However, complications of a carotid endarterectomy can be devastating and sometimes irreversible. Fortunately death is infrequent and often secondary to myocardial infarction. The benefits of carotid endarterectomy are largely based on the premise that complications are kept to a minimum. In instances where the complication rate of a centre is higher than the acceptable threshold the benefit of carotid endarterectomy may no longer be warranted.

Complications associated with carotid endarterectomy include neurological, cardiac and, as with any surgical procedure, generic complications occur in form of: anaesthetic related, respiratory, bleeding and infection. The specific complications of nerve injury, cerebral hyper perfusion syndromes and carotid restenosis will be discussed in more detail.

Myocardial & Haemodynamic complications

Coronary complications are the leading culprit of all carotid endarterectomy complications. It is believed that myocardial infarction (MI) may occur between a quarter to half of all the perioperative deaths and is the most common cause for late deaths2,3. Upto half of the patients undergoing carotid endarterectomy have symptomatic coronary artery disease (CAD)4. Despite these findings the perioperative cardiovascular event rates are on a decline. This change in status quo appears to be driven by improved medical management of these patients.

Haemodynamic instability may be considered a ‘symptom’ of surgery rather than a complication, but because postoperative haemodynamic instability after carotid endarterectomy may be linked to the surgery itself it is prudent to discuss it as a complication. The carotid sinus baroreceptors inhibit sympathetic activity when stimulated. 119

Evidence suggests that endarterectomy of the atherosclerotic plaque that is found at the bifurcation of the carotid artery creates a heightened sensitivity to baroreceptor mechanism that leads to decreased central nervous system sympathetic activity and results in bradycardia or hypotension or a combination of these5,6. The hypotension mediated through these mechanisms usually occurs within 2 hours of the operation. Intraoperative infiltration at the carotid sinus has been shown to reduce the occurrence of this complication7. On the other side of the spectrum post-operative hypertension (HPT) is associated with preoperatively elevated blood pressure. A hypothesis implicates denervation of the carotid sinus as the cause of this post-operative HPT. Recently the validity of the hypothesis has been questioned and other mechanisms, including cerebral noradrenaline and renin release have been looked at7,8,9,10. This HPT response normalises in up to 80% of individuals within 24 hours postoperatively.

In contrast to this early haemodynamic changes is the cerebral hyper perfusion syndrome, which occurs within several days postoperatively. The reported incidence ranges between 0.4 – 7.7% after a carotid endarterectomy and is often preceded by a severe headache and is hallmarked by significant HPT and acute neurological deficit. The most devastating consequence is an intracerebral haemorrhagic stroke and mortality rates of the HPS reach 75-100% for the severe cases. The aetiology appears to be ineffective cerebral blood flow calibration secondary to a carotid stenosis which has been relieved with the carotid endarterectomy. HPS appear to be more frequent in patients with high grade contralateral carotid stenosis and in patients who undergo surgery for contralateral high grade stenosis within 3 months of the index carotid endarterectomy for the ipsilateral stenosis11. SVS guidelines recommend a strict blood pressure control in the postoperative period, not exceeding SBP 140mmHg and DBP 80 mmHg12.

Neurological Complications

Neurological complications can be divided into ischemic strokes and local nerve injuries, nerve injuries being the more frequent of the two. The rate of 30 day stroke/ death in the original symptomatic trials was 5.8-6.7% and 7.5% in the NASCET 13 and ECST trials respectively. These stroke rates, of course, were lower in the asymptomatic patients, as is seen in the ACAS (2.3%) and ACST (3.1%) trials. In the more recent CREST trial the 30 day post-operative strike rate in the carotid endarterectomy group was 3.2%. 215 The strokes which occur intraoperatively or in the immediate postop period may be diagnosed promptly and have the potential to be treated with catheter directed thrombolytic agents. Flow must be restored within 1-2 hours to ensure success. Riles at al examined the rate of perioperative strokes in their series and divided them into categories. The overall perioperative stroke rate was 2.2% and six categories were identified14.

1. Ischemia during clamping, 2. Postoperative thrombosis and embolization, 3. Intracranial haemorrhage, 4. Stroke from other mechanisms related to surgery, 5. Strokes unrelated to reconstructed artery, 6. Unknown. Cranial nerve dysfunction incidence varies considerably, namely 5-20% as seen in retrospective studies. Unfortunately the different series have heterogeneous groups and direct comparison is difficult. The description of dysfunction is also not standardised in these studies. CREST trial cites an incidence of 4.7% of cranial nerve injury. This dysfunction is often transient and resolves at different time points. In one study all injuries resolved within 5 months and in another almost all deficits were gone within 12 months of the carotid endarterectomy. Cunningham et al, investigator for the ECST trial cited a rate of 0.5%

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permanent cranial nerve damage in the trial. In a paper by Schauber et al. the permanent cranial nerve damage was 1.1% of patients.

Cranial nerve injury is rarely from the structure being severed but most often related to blunt injury related to the dissection. Stretching and retraction of the tissues inadvertently stretches a nerve and may result in dysfunction. An increased incidence of CN injuries has also been shown in cases where the carotid endarterectomy takes longer than 2 hours15.

Injuries to branches of the cervical plexus are frequently unavoidable and occur with the skin incision. The transverse cervical nerve (C2 and C3) exits near the anterior border of the sternocleidomastoid (SCM) muscle and supplies cutaneous sensation to the anterolateral neck. Damage to this branch results in an insensate area medial to the incision16. The greater auricular (C2 and C3) nerve exits the SCM muscle, then ascends the upper neck to supply sensation to the skin overlying the inferior parotid gland and the lower earlobe.

Facial nerve is almost never damaged unless extensive manoeuvres for a high bifurcation have to be used. However, branches of the facial nerve are at risk. The first branch, cervical, gives motor innervation to the platysma muscle. This nerve is routinely sacrificed without postoperative disability. A second branch, the marginal mandibular nerve, courses inferior and parallel to the edge of the mandible to supply facial muscles responsible for maintaining proper function of the lateral mouth. Injury results in a lower lip droop on the ipsilateral side and usually occur from retraction. Recovery of neuropraxia in almost universal.

Cranial Nerve IX: Glossoharengeus The glossopharyngeal nerve is found high in the neck, running between the internal and external carotid arteries. It is injured during high dissection of the internal carotid artery. The nerves of Herring (or DeCastro), which supply the carotid sinus, are branches of the ninth cranial nerve.

Vagus (CN X) The vagus nerve usually descends the neck posterolateral to the carotid artery and posteromedial to the internal jugular vein. Injury to the vagus nerve and its branches are the most commonly injured clinically important nerves. Most injuries to the main vagus trunk are clamp related. A branch of the vagus nerve, the superior laryngeal nerve, travels with the superior thyroid artery. The nerve is frequently adherent to the posterior portion of this artery. This nerve supplies motor innervation to the cricothyroid muscle, denervation results in difficulty singing and talking, with limitations on high notes. A second branch of the vagus nerve, the recurrent laryngeal nerve, is rarely injured during a carotid endarterectomy. However, the possibility of a "nonrecurrent" recurrent laryngeal nerve must be kept in mind.

Spinal accessory nerve (CN XI) The spinal accessory nerve exits the base of the skull through the jugular foramen and courses beneath the posterior belly of the digastric and SCM muscles to supply innervation to the SCM and the trapezius. Injury results in complete paralysis of the SCM muscle and partial paralysis of the trapezius muscle. Deficits are noted by the presence of a winged scapula and difficulty in raising the shoulder.

Hypoglossus nerve (CN XII) The hypoglossal nerve should be identified during a carotid endarterectomy dissection. Its course is usually above the bifurcation and anterior to the internal and external carotid arteries. Frequently it is tethered down by an artery and vein to the SCM muscle. Division of the hypoglossal nerve produces ipsilateral deviation of the tongue and can be quite debilitating causing trouble with speech, eating, and drinking. Fibers of the hypoglossal 121

nerve descend joining fibers of Cl to form the anasa cervicalis. Division of this nerve is done with impunity leaving no obvious loss of function.

Bleeding and Infection

Comlications associated with infection are uncommon. Reported incidence of wound infection ranges from 0.09 – 0.15%. This is probably attributed to the generous blood supply in the neck. Increased infection with prosthetic patch, while theoretically proposed, has not been shown. Many surgeons are changing over to the use of bovine pericardium patches and these are thought to be very resistant to infection.

Postoperative bleeding is mostly attributed to capillary oozing and associated with perioperative antiplatelet use and heparin administration intraoperatively. Haemorrhage is uncommon and reported incidence ranges between 0.7-3%17.

Restenosis

Late complications in form of carotid artery restenosis are known to occur in 5-22% of patients. Importantly, it appears that only 3 % of these are symptomatic18. Recurrent stenosis develop more frequently in female patients, patients who [persist with smoking, poorly controlled HPT, high cholesterol and diabetes mellitus. Restenosis may be divided into early, < 2 years and late more than 2-3 years. The early restenosis is secondary to neointimal hyperplasia (NIH) and has less likelihood of ulceration or thrombosis as it does not exhibit the typical atherosclerotic plaque surface characteristics. NIH has also been shown to regress in up to 35% of cases. A surgeon should have a high threshold for reintervention for restenosis and should be reserved for very high grade lesions or unstable lesions. Treatment modalities include CAS or carotid endarterectomy with weak data to support each modality of treatment. Albeit both carry higher risks than the initial carotid surgery.

Conclusion

Current literature supports the use of endarterectomy for carotid stenosis in patients with the appropriate indications. Because of the fact that most perioperative strokes occur as a result of technical imperfections, meticulous care must be given to all aspects of the procedure and medical perioperative management optimised in order to avoid potentially devastating complications. Detailed knowledge of anatomy is required to prevent surgical ‘mishaps’ and especially inadvertent local nerve injury. Restenosis is often clinically asymptomatic and repeat corrective procedures must be carefully considered on individual patient basis.

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References

1. Moore WS. In Rutherford RB, et al. (eds). Vascular Surgery, 5th edn. Vol 2. Philadelphia: W.B. Saunders Company 2000:1713-1730. 2. Kazmers A et al.: The role of perioperative radionucleotide left ventricular ejection fraction for risk assessment in carotid surgery. Arch Surg. 123:416-419 1988 3. Hertzer NR, et al.: Fatal MI following CEA in 335 patients. Ann Surg. 194:212-218 1981 4. Nunn DB: Carotid endarterectomy: an analysis of 234 operative cases. Ann Surg. 182:733-738 1975 5. Pine R et al.: Control of post carotid endarterectomy hypotension with baroreceptor blockade. Am J Surg. 147:763-765 1984 6. Lehv MS et al.:Hypertension complicating carotid endarterectomy. Stroke. 1:307-313 1970 7. Angell-James JE et al. : The effects of CEA on the mechanical properties of carotid sinus and carotid nerve activity in atherosclerotic patients. Br J Surg. 61:805-810 1974 8. Towne JB et al. The relationship of postoperative hypertension to complications following carotid endarterectomy. Surgery. 88:575-580 1980 9. Hertzer NR et al.: Surgical staging for simultaneous coronary and carotid disease. J Vasc Surg. 9:455-463 1989 10. Takach TJ et al.: Is an integrated approach warranted for concomitant carotid and coronary artery disease? Ann Thorac Surg. 64:16-22 1997 11. Ascher e et al. Cerebral hyperperfusion syndrome after carotid endarterectomy. J Vasc Surg. 37:769-777 2003 12. Ricotta JJ et al: Updated Society for Vascular Surgery guidelines for management of extra cranial carotid disease: executive summary. J Vasc Surg. 54:832-836 2011 13. Beneficial effects of carotid endarterectomy in symptomatic patients with high grade stenosis. NASCET Collaborators. N Engl J Med. 325:445:453 1991 14. RilesTS, Imparato AM, et al. The cause of perioperative stroke after carotid endarterectomy. J Vase Surg 1994; 19:206-216. 15. Binaghi S et al. Three-dimensional computed tomography angiography and magnetic resonance angiography of carotid bifurcation stenosis. Eur Neurol. 46:25-34 2001 16. BryantMF. Complications associated with carotid endarterectomy. Am Surg 1976; 42:665-669. 17. Magarenelli N et al. Carotid stenosis: comparison between MR and spiral CT angiography. Neuroradiol. 40:367-373 1998 18. Sadideen H, et al: Restenosis after carotid endarterectomy. Int J Clin Pract. 60:1625- 1630 2006

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ARE SURGEONS VIGILANT ENOUGH FOR THROMBO-EMBOLIC DISEASE? Y-N S.C Tsotetsi: Vascular Surgeon

Introduction

Acute DVT is a common disease with potentially life-threatening consequences and long- term life-altering complications. It imposes huge economic burden on the society. The disease is difficult to diagnose because of the lack of sensitivity and specificity of its clinical manifestations. Diagnostic algorithms are needed for safe and effective diagnosis. The treatment is standard anticoagulation therapy which reduces significantly the mortality risk and recurrence of the disease but does a poorer job when it comes to the long-term morbidity of the disease. Active management of acute of acute DVT, especially proximal iliofemoral DVT, using catheter directed thrombolysis with or without mechanical thrombectomy modalities is gaining momentum and may prove to be the standard therapy of the future as it adds to the standard therapy the significant reduction of the long term morbidity specifically post thrombotic syndrome.

Etio-pathogenesis

In 1860, Rudolf Virchow described the famous triad of factors that are still considered the main factors in the pathogenesis of venous thrombosis.

Natural History

The relative balance between organization, thrombolysis, propagation and rethrombosis determines the outcome of human acute DVT. Venous duplex ultrasound which permits individual venous segments to be observed over time has documented that recanalization does occur in most patients after an episode of acute DVT. Van Ramshorst and associates found that most recanalizations occur within the first 6 weeks, with flow re-established in 87% of cases. Killewiand colleagues reported a linear decrease in thrombus load, and by 24 – 36 weeks, only 26% of the original thrombus remained. However, recanalization may continue albeit at a slower rate for months to years after an acute event. Rethrombosis has also been reported in the affected segments. The incidence of recurrent thrombosis is 5.2% of those who were treated with standard anticoagulation for 3 months compared with 47% in those who were inadequately treated.

Complications

Pulmonary embolism (PE) is the most devastating complication of acute DVT. The majority of these incidents are clinically silent. Recent studies have shown that in patients with symptomatic acute DVT of the lower extremity, 50 – 80% develops asymptomatic PE. It was also found that symptomatic PE complicates 17% of patients with proximal upper extremity acute DVT. Patients with symptomatic PE have 18 times the mortality rate compared with patients with acute DVT alone. Patients who survive the acute PE event are still at risk of development of chronic thromboembolic pulmonary hypertension

Post thrombotic Syndrome (PTS) is a group of clinical manifestations in patients who have history of acute DVT due to ambulatory venous hypertension in their affected limbs. It is the most common late complication of acute DVT and is responsible for a greater degree of 124

greater of chronic socioeconomic and quality of life morbidity. The cause of ambulatory venous hypertension is a combination of venous reflux secondary to valvular incompetence and residual luminal obstruction.

Diagnostic strategy

Although duplex ultrasound is extremely accurate in the diagnosis of acute DVT, its overuse in the evaluation of patients with suspected acute DVT imposes intense burden on the hospital resources. The suspicion of acute DVT in hospitalised patients requires confirmatory testing, usually duplex ultrasound due to the high pre-test probability of the disease in that population.

The situation is different in the outpatient setting where the prevalence of the disease and hence the pre-test probability are much lower. In those patients, the first step is to stratify their pre-test probability for the presence of acute DVT using one of the available risk stratification scores, commonly the Wells score. Patients with low and intermediate probability are exposed to D-dimer testing. In case it is negative, that essentially excludes the diagnosis of acute DVT. On the other hand, patients with high probability for DVT will require duplex ultrasound.

Treatment

The therapeutic goals of treatment of acute DVT of the lower extremity include prevention of clot extension and possible resultant PE and relief of lower extremity pain and swelling as a consequence of venous obstruction. The long term goals include preservation of venous valvular function and patency to prevent the development of PTS

The contemporary management of acute lower extremity DVT includes these alternatives

1. Standard anticoagulation alone 2. The use of thrombolytic therapy in conjunction with anticoagulation 3. Endovenous thrombectomy using designed to mechanically remove the thrombus combined with thrombolytic therapy in addition to anticoagulation 4. The use of iliac stenting in patients with iliac stenosis 5. Inferior vena cava filters in patients with a contraindication to anticoagulation estimate for recurrent VTE was imprecise. The American College of Chest Physicians current guidelines recommend the placement of an inferior vena cava filter in patients with documented VTE or PE and a contraindication to anticoagulation, complications of bleeding as a result of anticoagulation, failure of anticoagulation, or VTE despite therapeutic anticoagulation. 6. Compression stockings applying an ankle pressure of 30 to 40 mm Hg and a lower pressure higher up the leg (i.e., graduated pressure) should be started as soon as feasible after starting anticoagulant therapy. 7. Thromboprophylaxis, either mechanical or pharmacologic is recommended according to the patient’s risk

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References

1. Patterson BO, et al. indications for catheter-directed thrombolysis in the management of acute proximal deep vein thrombosis. Arterioscler Thromb Vasc Biol.2010;30(4):669-74 2. Prandoni P, et al. The long-term clinical clinical course of acute deep venous thrombosis. Ann Intern Med. 1996; 125(1):1-7 3. Kakkar VV, et al. Natural history of postoperative deep-vein thrombosis. Lancet. 1969; 2(7614); 230-2. 4. Wakefield TW, Myers DD, Henke PK. Mechanisms of venous thrombosis and resolution. Arterioscer Thromb Vasc Biol. 2008;28(3):387-91 5. Killewich LA, et al. Regression of proximal deep venous thrombosis is associated with fibrinolytic enhancement. J Vasc Surg. 1997;26(5):861-8 6. Pengo V, et al. Incidence of chronic thromboembolic pulmonary hypertension after pulmonary embolism. N Engl J Med. 2004; 350(22):2257-64. 7. Kahn SR, et al. Determinants of health-related quality of life after during the 2 years following deep vein thrombosis. J Thromb Haemost. 2008;6(7):1105-12 8. Enden T, et al.Catheter-directed Venous Thrombolysis in acute iliofemoral vein thrombosis – the CaVenT Study: Am Heart J.2007;154(5):808-14 9. Kearon C, et al. Antithrombotic therapy for venous thromboembolic disease: American College of Chest Physicians evidence-based clinical practice guidelines (8th edition). Chest.2008; 133(6 suppl):160S-98.

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This presentation will deal briefly with (a) the present situation in public health sector regarding treatment for deep vein thrombosis to prevent pulmonary embolism; (b) the problems of procurement in the public sector; (c) general principles regarding medical practice in a resource-starved environment; (d) when healthcare practitioners will be liable for negligence or malpractice; (e) when healthcare administrators will be liable for negligence; (f) vicarious liability; and (g) when healthcare practitioners can be absolved. The participants will then be given a scenario to discuss.

The present situation in public health sector regarding treatment for deep vein thrombosis (DVY) to prevent pulmonary embolism (PE).

Research indicates that PE arising from DVT accounts for 10% of all hospital deaths. VTE prophylaxis is used to prevent DVT and subsequent PE. Patients are assessed using patient-related and procedure-related risk factors. Patient’s undergoing low-risk procedures with no patient-related risk-factors, require no specific prophylaxis. Patient’s undergoing low- risk procedures with additional patient-risk factors, or those undergoing higher-risk procedures with or without patient-related risks, are put on a LMWH according to the risk classification in the protocol. (see generally, BF Jacobson et al ‘Venous thromboembolism – prophylactic and therapeutic practice guideline’ (2009) 99(6) SAMJ 467-473)). For very high- risk procedures attempts are made to arrange intermittent compression devices (IVD) to be applied in theatre and used until the patient is mobile – but IVDs are not always available. The use of IVDs is based on surgeon preference and is not in the protocol.

Problems of procurement in the public sector

IVDS and the necessary consumables are ordered and supplied by the procurement department of the hospital.

Stock controllers are supposed to check and ensure the availability of consumables and other relevant stock such as LMWHS and IVDS. Usually LMWHS are ‘readily available and used frequently’. IVDS are not readily available. Often there is a stock problem and the correct consumables are not available because the items have not been ordered or the budget has been overspent.

General principles regarding medical practice in a resource-starved environment

In a resource-deficient environment, liability for medical malpractice depends on whether there was intentional or negligent wrongful conduct by the parties concerned. Where the department of health is involved, vicarious liability will depend on whether its employees were acting in the course and scope of their employment when they committed the wrongful acts or omissions. Departments of health and public sector hospitals may be liable for the

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wrongful conduct of their healthcare service staff as well as their administrators and managers.

Departments of health and public hospitals will be vicariously liable for the intentional or negligent wrongful acts or omissions of their clinical health care and support staff acting in the course and scope of their employment. The department of health and public hospitals will be liable for harm caused to patients arising from a shortage of resources due to intentional or negligence conduct by their administrative employees.

When healthcare practitioners will be liable for negligence or malpractice

Healthcare practitioners are expected to exercise the degree of skill and care of reasonably competent practitioner in their particular branch of profession. (Castell v De Greef 1993 (3) SA 501 (C)). The more complicated the procedures the greater the skill and care that must be exercised - within available resources. (Collins v Administrator,Cape 1995 (4) SA 73 (C)). The test for negligence is whether a reasonably competent practitioner in the position of the defendant ought to have foreseen the likelihood of harm and guarded against it. A failure to exercise the required degree of skill and care resulting in injury and damage to a patient will result in a claim for professional negligence. An intentional wrongful act against a patient will result in a claim for malpractice (eg. breach of confidence; failure to obtain an informed consent).

When healthcare administrators may be held liable for negligence or maladministration

Healthcare administrators are expected to exercise the degree of skill and care of reasonably competent people in their position in the organisation. The test for negligence is whether a reasonably competent person in the position of the administrator ought to have foreseen the likelihood of harm and guard against it. Thus administrators who intentionally overspend their budgets due to engagement in unlawful tender transactions; wasteful expenditure on travel, entertainment and study tours; or the overuse of consultants etc. May be guilty of maladministration. Other examples are negligently failing to repair or replace medical equipment, or to order medical items and drugs when funds are available, or diverting funds from health care services to the detriment of patients. (D McQuoid-Mason ‘Establishing liability for harm caused to patients in a resource-deficient environment’ (2010) 100(9) SAMJ 573-575).

Vicarious liability

Vicarious liability means that one person is liable for another person’s wrong act even though the first person is not at fault. Vicarious liability applies where a person employs another as a ‘servant’ and the latter unlawfully harms a third person while acting ‘within the course and scope of their employment’. Subject to the above, departments of health may be liable for wrongs committed by people employed by them whether they act negligently or intentionally. The employees – whether health care service practitioners or administators may also be held liable personally. Health care practitioners and administrators are not liable

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for the acts of independent contractors contracted by them – unless they negligently failed to prevent the harm. (cf S v Kramer 1987 (1) SA 887 (W)).

When health care practitioners can be absolved

Health care practitioners can be absolved from liability:

– Where they did not negligently or intentionally cause harm to the patient or anyone else;

– Where they are faced with an emergency situation and have acted reasonably outside their speciality because nobody else is available to assist – they will be judged by the standard of how a reasonably competent practitioner with their skill and experience would have acted in the same situation;

– Where they are faced with a shortage of resources such as drugs or equipment, if they acted in the way a reasonably competent person in their branch of the profession would have acted in the same situation;

– Where a ‘material risk’ against which a patient was warned manifests itself and there was no negligence by the health care practitioner.

[Note: Both health care practitioners and administrators they may be held jointly and severally liable to the injured persons in which case damages will be apportioned].

Scenario

A healthy, active, 40 year patient presents at a State hospital emergency room complaining of shortness of breath on exertion and chest pain. He is subjected to (a) a non-stress test (during which he fainted); (b) a CT scan without contrast (‘because it would be too hard on his kidneys’); (c) a D-Dimer blood test (which was abnormal and elevated); (d) a V/Q perfusion lung scan (in which part of his lungs were hidden by his arms and the radiologist interpreted as ‘low probability of PE’); and (e) an echocardiogram (indicating massive enlargement of the right ventricle and right atrium, pulmonary hypertension, and moderate Tricusbid regurgitation). A cardiologist and pulmonologist are consulted.

The cardiologist after seeing the other test results, relies soley on the V/Q scan and diagnoses obstructive sleep apnea. The pulmonologist does not examine the echocardiogram and diagnoses asthma and obstructive sleep apnea and like the cardiologist indicates that the results of the V/Q scan are sufficient to rule out pulmonary embolism. The patient’s discomfort continues and at another hospital he is diagnosed as having a ‘massive’ PE and has to have an interior vena cava filter inserted. He continues to suffer from shortness of breath and can no longer work. Were the cardiologist and pulmonologist negligent? Why or why not? If they were, would the State be vicariously liable for their negligence?

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