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Case Report Thoracic Trauma and Post Operative Lung Injury in a Neonatal Foal A

Case Report Thoracic Trauma and Post Operative Lung Injury in a Neonatal Foal A

186 EQUINE VETERINARY EDUCATION / AE / april 2009

Case Report Thoracic trauma and post operative in a neonatal foal A. Borchers, A. van Eps†, S. Zedler‡ and P. A. Wilkins* Department of Clinical Studies Sections of Emergency, Critical Care and ; †Medicine; and ‡Surgery, University of Pennsylvania, School of Veterinary Medicine, New Bolton Center, Kennett Square, Pennsylvania, USA.

Keywords: horse; rib fractures; parenchymal pulmonary disease

Summary are characterised by noncardiogenic pulmonary oedema and pulmonary resulting in acute respiratory A 24-hour-old Standardbred filly was referred with an dysfunction (DeClue and Cohn 2007; Wilkins et al. 2007). acute history of weakness, respiratory distress and There are no prior reports in the literature detailing . Radiographic evaluation pulmonary injury in neonatal foals after thoracic trauma. revealed left sided rib fractures, unilateral This Case Report discusses pulmonary injury based on serial and pneumomediastinum. Serial arterial blood gas arterial blood gas (ABG) analyses, consecutive thoracic measurements pre- and post rib repair showed pulmonary radiographs and the medical management of a neonatal dysfunction. Post operative radiographs revealed the foal with rib fractures and evidence of impaired presence of air bronchograms and a bronchointerstitial pulmonary function before and after surgical repair. pattern, suggestive of alveolar parenchymal pathology consistent with pulmonary contusion, pulmonary oedema Case details or ALI/ARDS. The filly was treated with intranasal and an active chest draining unit and recovered History uneventfully. A one-day-old Standardbred filly, born to a multiparous Introduction mare at 338 days of gestation, presented with a history of weakness, respiratory distress and diffuse subcutaneous Severe thoracic injury with post traumatic parenchymal emphysema over the left neck and . Stage 2 labour lung disease influences morbidity and mortality in human was prolonged and lasted 45 min. The filly was delivered trauma patients (Keel and Meier 2007). Thoracic injury in via assisted vaginal delivery that included manipulation veterinary medicine includes penetrating chest wounds and traction applied to the thoracic limbs. Following (Hance and Robertson 1992; Hassel 2007), rib fractures delivery the foal was apnoeic and required (Jean et al. 1999, 2007; Bellezzo et al. 2004; Kraus et al. cardiopulmonary (CPR). Resuscitation was 2005) and (Olsen et al. 2002) resulting in successful but the filly was slow to stand and to nurse. complications including subcutaneous emphysema, Serum IgG concentration (IgG) 12 h after parturition was pneumothorax, pneumomediastinum, haemothorax, greater than 8 g/l. Over the next 24 h the filly became diaphragmatic hernia, pulmonary collapse and contusion, obtunded, weak and tachypnoeic. Diffuse subcutaneous myocardial lacerations and punctures and emphysema over the left neck and thorax became haemopericardium (Hance and Robertson 1992; apparent. The foal received 1 litre of Normosol-R1, i.v., Schambourg et al. 2003; Hassel 2007; Keel and Meier procaine-penicillin (1017 iu/kg bwt, i.m. once) and 2007). Acute lung injury (ALI) and acute respiratory distress gentamicin (0.6 mg/kg bwt, i.v., once) from the farm syndrome (ARDS) are secondary inflammatory responses manager prior to referral. to multiple lung injury including thoracic trauma. ALI/ARDS Clinical findings

*Author to whom correspondence should be addressed. Present address: Department of Veterinary Clinical Science, 1008 West On presentation the filly was recumbent and depressed, Hazelwood Drive, Urbana, Illinois 61802, USA. with a body condition score of 4/9 and a bodyweight of EQUINE VETERINARY EDUCATION / AE / april 2009 187

TABLE 1: Arterial blood gas results during hospitalisation

Hours after initial presentation Preoperatively Post operatively Hours 0 1.5 2 4 7.5 12 22 34 41 60 75 84 109

INO2 (l/min) RA 10 10 10 10 10 8 6 RA RA 3 RA RA pH 7.35 7.29 7.35 7.36 7.32 7.31 7.40 7.33 7.39 7.48 7.49 7.46 7.48 PaO2 (mmHg) 44.9 142 124 50.6 94.5 57.6 168 133 55.9 61.5 116 63.5 72.3 PaCO2 (mmHg) 63.4 75.9 65.6 61.7 69.9 72.6 51.7 69.2 57.6 48.4 45.9 48.9 43 O2Sat (%) 74.8 99.1 98.8 81.6 96.4 84.8 99 98.9 86.8 92 99.1 92.3 95.1 PaO2/FiO2 213 266 292 302 344 PAO2 (mmHg) 65 75.4 86.3 86.7 94.3 PAO2 - PaO2 20.1 19.5 24.8 23.2 22

INO2 = intranasal oxygen; PaO2 = partial pressure of oxygen in arterial blood; PaCO2 = partial pressure of in arterial blood; O2Sat = ; FiO2 = fractional inspired oxygen concentration; PAO2 = partial pressure of oxygen in the alveolar gas; RA = room air.

59 kg. Moderate flexor tendon laxity was present in all subcutaneous emphysema. Bronchovesicular lung sounds limbs. The mucous membranes were pink and moist with a were auscultated over the right hemithorax. The refill time of 2 s. Peripheral pulse quality was strong remainder of the was unremarkable. and the distal extremities and ears were warm to the The foal was moderately haemoconcentrated at touch. Other physical examination findings included admission (packed cell volume 46%, reference range [rr] severe diffuse subcutaneous emphysema over the left 30–42%) and plasma fibrinogen concentration was mildly neck, thorax and abdomen with painful responses increased at 3.3 g/l (rr 1–3 g/l). Plasma IgG concentration localised to the left mid thoracic area. Thoracic was 8.3 g/l. Other plasma clinical chemistry abnormalities auscultation revealed (100 beats/min), included increased creatinine-kinase activity at 12,339 u/l a restricted, shallow, periodic pattern at (rr 90–270 u/l) and increased total bilirubin concentration 24 breaths/min and a rectal temperature of 38.9°C. A at 117 µmol/l (rr 1.7–32.5 µmol/l). A blood culture obtained grade 1/6 systolic murmur and a ‘mechanical clicking’ on admission was negative for bacterial growth. Arterial were auscultated over the right base. Auscultation blood gas (ABG) analysis obtained in lateral recumbency of left heart and thorax was not possible due to on room air revealed hypercapnia, hypoxaemia and an oxygen saturation of 74.8% (Table 1). Thoracic radiographs in right lateral recumbency revealed a diffuse interstitial to alveolar pattern, subcutaneous emphysema, unilateral (left) pneumothorax,

Fig 1: Thoracic radiograph of a neonatal foal with diffuse subcutaneous emphysema, pneumomediastinum and pneumothorax in right lateral recumbency. There is air contrast around the oesophagus and trachea and caudal displacement Fig 2: Caudo-dorsal radiographs of the same foal in right lateral of the cardiac silhouette indicating pneumomediastinum recumbency. Note the outline of the collapsed dorsal margin of (black arrows). the left lung lobe (white arrows) indicating pneumothorax. 188 EQUINE VETERINARY EDUCATION / AE / april 2009

pneumomediastinum and fractures of ribs 8–9 of the left hemithorax (Figs 1 and 2). Ultrasonographic imaging of the fractured ribs of the left hemithorax was attempted but unsuccessful due to the extent of the subcutaneous emphysema; ultrasonographic examination of the right hemithorax showed normal lung tissue, normal cardiac structures and no evidence of . A problem list after the initial evaluation included recumbency, rib fractures of the left hemithorax, pneumothorax, pneumomediastinum, diffuse subcutaneous emphysema over the left neck, thorax and abdomen, diffuse interstitial to alveolar pattern on thoracic radiographs, hypoxaemia and hypercapnia.

Case management

To relieve the pneumothorax a teat cannula was placed caudodorsally using sterile technique between the 10th and 11th ribs and 250 ml of air was manually evacuated with a syringe. An ABG obtained immediately prior to aspiration demonstrated respiratory acidosis with moderate hypercapnia (Table 1, 1.5 h). An ABG obtained Fig 3: Thoracic radiographs taken immediately post operatively in after aspiration of air from the thorax showed an improved right lateral recumbency show moderate to severe diffuse bronchointerstitial and alveolar pattern. PaCO2 with resolution of the respiratory acidosis (Table 1, 2 h). Further treatment included placement of a 16 gauge maintained with sevoflurane10 in oxygen. During left jugular vein catheter2 under sterile conditions and anaesthesia the filly was hypoventilating and was therefore administration of 5% dextrose in water1 i.v., at 4 mg maintained on positive pressure dextrose/kg bwt/min, intranasal O2 at 10 l/min (170 ml/kg with a positive end expiratory pressure of 4 cmH2O. bwt/min, intranasal cannula); 1 unit (900 ml) of Fractures of the 5th–11th ribs were identified at surgery. hyperimmune plasma3 for supplementation of There was severe disruption of the associated pleura and immunoglobulin, coagulation factors and anti-endotoxin displacement of the ventral fragments of the 6th–9th ribs effects; magnesium sulphate4 (10% solution at 42 mg/kg into the thorax. The 6th–11th rib fractures were repaired with bwt/h loading dose followed by 25 mg/kg bwt/h constant nylon monofilament suture as previously described (Kraus rate infusion) as a neuroprotectant; sucralfate5 (20 mg/kg et al. 2005). Recovery from anaesthesia was uneventful. bwt per os, q. 8 h) for gastric protection; and flunixin After surgery, the filly was treated with i.v. potassium- meglumine6 (0.5 mg/kg bwt i.v., q. 12 h) for analgesia and penicillin every 6 h, i.v. amikacin once daily and sucralfate, anti-inflammatory effects. Antimicrobial treatment per os, 3 times daily. Butorphanol (0.015 mg/kg bwt i.m., included amikacin7 (30 mg/kg bwt i.v., q. 24 h) and q. 8 h) was administered for analgesia for 48 h post potassium penicillin8 (3 x 104 iu/kg bwt i.v., q. 6 h). operatively. Intravenous Normosol-R and 10% dextrose in An ABG obtained 2 h following aspiration of air from water were administered as a constant rate infusion until the left hemithorax revealed moderate hypoxaemia and the foal was able to ambulate and nurse consistently from an indwelling thoracic tube (Argyle chest tube)9 was the mare. The filly was treated with intranasal oxygen placed for continuous thoracic evacuation and located supplementation at 6–8 l/min (102–135 ml/kg bwt/min, dorsally between ribs 10 and 11 (Table 1, 4 h). A follow-up intranasal cannula) and received one additional unit of ABG at 3.5 and 8 h after chest tube placement revealed plasma after surgery. persistent respiratory acidosis with hypercapnia and Further post operative management included an hypoxaemia (Table 1, 7.5 and 12 h). active chest drainage unit (Argyle Thora-Seal III)9 Due to concern for continued or exacerbated attached to the indwelling chest tube for continuous intrathoracic visceral trauma from displaced fragments of evacuation of air and fluid from the mediastinal and the fractured ribs, and continuous respiratory compromise, pleural cavities. The chest drainage unit was removed the decision was made to surgically repair the fractured 24 h post operatively as negative pressure within the ribs using a previously published nylon strand suture repair chest cavity was consistently apparent. Thoracic technique (Kraus et al. 2005). radiographs taken immediately post operatively showed Premedication included midazolam10 (0.2 mg/kg bwt moderate to severe diffuse bronchointerstitial and i.v.) and butorphanol7 (0.3 mg/kg bwt i.v.); anaesthesia was alveolar patterns consistent with pulmonary oedema or induced with ketamine7 (1.1 mg/kg bwt i.v.) and acute lung injury, possibly due to inflammation or EQUINE VETERINARY EDUCATION / AE / april 2009 189

Discussion

The filly in this Case Report suffered from severe trauma to the thorax during and following parturition and subsequent pulmonary dysfunction pre- and post operatively after rib fracture repair. Pneumothorax, , pulmonary oedema, pulmonary contusion and thoracic pain may have all contributed to the observed pulmonary dysfunction, and oxygenation deficit. Injury to the lung parenchyma can be devastating, leading to pulmonary failure and death. In man, pulmonary contusion is the most common intrathoracic injury encountered in nonpenetrating chest trauma (Miller et al. 2001). Pulmonary contusion can be complicated by pulmonary dysfunction, ALI and ARDS (Groeneveld 2007). Contusion volume is an independent predictor for development of ALI/ARDS and human patients with ≥20% pulmonary contusion carry an 82% increased risk of ALI/ARDS than those with <20% pulmonary contusion (Miller et al. 2001). ALI/ARDS is part of the systemic Fig 4: Standing lateral thoracic radiographs taken 6 days post inflammatory response syndrome (SIRS) to either direct or operatively show marked improvement of previous moderate to indirect initial stimuli, which can evolve to an uncontrolled, severe diffuse bronchointerstitial and alveolar pattern. self-perpetuating state. The acute phase of ALI/ARDS is characterised by: damage to the alveolar epithelium and contusion, or atelectasis (Fig 3). An ABG obtained 2 h pulmonary capillary ; migration post operatively, showed improved oxygenation and into injured endothelium, epithelium and alveoli; influx of resolved hypercapnia (Table 1, 22 h); however, 12 h later protein-rich oedema fluid into the alveoli; and respiratory acidosis with hypercapnia was again upregulation of proinflammatory cytokines, interleukins apparent. Thoracic auscultation at this time revealed (IL-1, 6, 8, 10) and tumour necrosis factor α (TNF-α) (Ware bronchovesicular lung sounds bilaterally and a respiratory and Matthay 2000). Clinical signs usually manifest as rapid rate of 20 breaths/min without increased respiratory onset of respiratory distress and arterial hypoxaemia that is effort. As the pleural evacuation unit was functioning refractory to treatment (Ware and Matthay 2000). Typical properly and the subcutaneous emphysema was slowly radiographic findings include patchy or asymmetric resolving, pneumothorax and/or pleural effusion was alveolar infiltrates and a bronchointerstitial pattern (Ware deemed to be less likely to be the cause of hypercapnia and Matthay 2000; Dunkel et al. 2005). The degree of and hypoventilation, and parenchymal lung disease was hypoxaemia, defined by the ratio of arterial oxygen considered a more likely cause. concentration to fractional inspired oxygen concentration

Three days after surgery the filly was ambulatory and (FiO2), differentiates between ALI/ARDS at <300 or active, nursing well with physical examination findings <200 mmHg respectively (Bernard et al. 1994). A recent within normal limits. Follow-up ABG samples obtained on consensus definition for veterinary ALI/ARDS grouped room air over the 3 days after surgery revealed resolving neonatal foals into a separate group (EqNALI/EqNARDS) hypercapnia and (Table 1, 41–109 h). Intranasal taking into account age-dependent adaption of the oxygen was discontinued on Day 3 after surgery. Follow-up PaO2/FiO2 ratio in neonatal foals in lateral recumbency radiographs obtained 5 days post operatively showed breathing room air (Wilkins et al. 2007). Accordingly, a marked improvement of the severe diffuse neonatal foal at 24 h of age would qualify for EqNALI/ bronchointerstitial and alveolar patterns with a persistent EqNARDS if the PaO2/FiO2 ratio is <200 or <140 mmHg, mild bronchointerstitial pattern (Fig 4). respectively (Wilkins et al. 2007). The foal remained stable, and antimicrobial therapy The foal in this Case Report suffered from thoracic was changed to doxycycline11 (10 mg/kg bwt per os, q. trauma in the form of multiple rib fractures during 12 h) on Day 5 of hospitalisation. The foal was discharged parturition followed by chest compressions applied during on Day 6 with instructions for a further 3 weeks of stall rest. CPR. Fractured rib fragments penetrated the thoracic cavity, leading to pneumothorax and diffuse Outcome subcutaneous emphysema on the left neck, thorax and abdomen. In this case pneumomediastinum was probably Follow-up telephone conversations one and 3 months after a sequela to pneumothorax and diffuse subcutaneous discharge indicated that the foal continued to do well. Six emphysema. The subcutaneous emphysema may have months after discharge the filly was sold at a yearling sale. migrated directly into the mediastinal space, or air 190 EQUINE VETERINARY EDUCATION / AE / april 2009

trapped in the may have penetrated the The foal responded favourably to initial chest visceral pleura of the lung and the parietal pleura of the evacuation to relieve the pneumothorax, demonstrating mediastinum (Hance and Robertson 1992). Serial arterial increased oxygenation and decreased hypercapnia blood gas measurements pre- and post operatively (Table 1, 2 h). Two hours after chest evacuation, however, showed pulmonary dysfunction in the form of hypoxaemia oxygen saturation decreased to 81.6% with hypoxaemia and hypercapnia. despite intranasal oxygen at 10 l/min (Table 1, 4 h). Chest Reasons for observed hypoxaemia may include low radiographs were not obtained at that point and it is

FiO2, ventilation- (V/Q) mismatch in the form of unclear if persistent or recurrent pneumothorax, or other increased dead space ventilation or venous admixture complications such as re-expansion pulmonary oedema, (intrapulmonary shunt), hypoventilation or imbalances of caused the diminished pulmonary function. Re-expansion oxygen delivery (DO2) and oxygen uptake (VO2). pulmonary oedema is a rare complication reported in Observed hypercapnia may also be explained by human medicine, which occurs after thoracic drainage hypoventilation and V/Q abnormalities (Marino 2007). for pneumothorax or pleural effusion (Tariq and Sadaf

Low FiO2 was unlikely in this case. Therefore we 2006; Conen et al. 2007; Neustein 2007). Radiographically, evaluated the PaO2/FiO2 ratio which is an indirect re-expansion pulmonary oedema is indistinguishable from measure of shunt fraction (fraction of that ALI/ARDS and atelectasis, as both conditions will cause is intrapulmonary shunt or venous admixture). diffuse alveolar infiltrates and a bronchointerstitial pattern

Initial PaO2/FiO2 ratio was 213 mmHg and would have on radiographs. Computed tomography may help to qualified the foal for ALI according to the guidelines differentiate between re-expansion pulmonary oedema, published for human medicine but not according to the ALI/ARDS or atelectasis but was not available in this case new consensus definition for EqNALI/EqNARDS (Bernard (Scillia et al. 2004). Radiographs, taken immediately post et al. 1994; Wilkins et al. 2007). Alternatively atelectasis due operatively, showed a severe diffuse bronchointerstitial to pneumothorax and pulmonary contusion may have and alveolar pattern consistent with pulmonary oedema damaged sufficient pulmonary volume to cause enough or acute lung injury possibly due to inflammation, V/Q mismatch in the form of an intrapulmonary shunt to contusion or atelectasis. However, radiographs obtained meet human guidelines for ALI with respect to the PaO2/ 6 days post operatively showed marked improvement of FiO2 ratio. This is also supported by a recent publication in the severe diffuse bronchointerstitial and alveolar patterns the human literature that evaluated and compared lung with a persistent mild bronchointerstitial pattern indicating capillary protein permeability and extravascular lung mild residual injury. water in human trauma patients following invasive surgery Treatment for ALI/ARDS remains supportive and, in (Groeneveld 2007). Results suggested that pulmonary severe cases of hypoxaemia and respiratory distress, dysfunction and radiographic changes in patients with includes mechanical ventilation with low tidal volumes ALI/ARDS after trauma and surgery are likely to be due in (5–6 ml/kg bwt) and positive end expiratory positive part to atelectasis rather than permeability oedema pressure (Ware and Matthay 2000). Fluid therapy should be (Groeneveld 2007). restricted to avoid pulmonary oedema and frusemide At least 2 other causes of hypoxaemia were possible in continuous rate infusion has been recommended in this foal: hypoventilation and DO2/VO2 imbalance (Marino human patients with ALI/ARDS (Reising et al. 1999), with an 2007). Hypoventilation - defined by increased PaCO2 - in aim of maintaining a mild negative . Diuresis this case due to neonatal encephalopathy, thoracic pain is also recommended for the treatment of re-expansion or parenchymal disease, was evidenced by an initial pulmonary oedema (Neustein 2007). Further supportive rate of 24 breaths/min in the face of moderate treatment may include the administration of nitric oxide or hypoxaemia and hypercapnia. Pure alveolar other vasodilators, and administration of glucocortocoids hypoventilation, however, results in a normal alveolar– or other anti-inflammatory agents (Ware and Matthay arterial (A-a) PO2 gradient, which is an indirect measure of 2000). The filly in the present Case Report received i.v. V/Q abnormalities (Marino 2007). The A-a PO2 gradient fluids at a maintenance rate pre- and post operatively to was increased in our foal, indicating V/Q mismatch avoid overhydration and pulmonary oedema. Positive probably related to pneumothorax and pulmonary pressure mechanical ventilation and positive end atelectasis. V/Q abnormalities will usually not increase expiratory pressure support was required during

PCO2, unless the condition is very far advanced; therefore, anaesthesia. After surgery the filly’s ability to oxygenate a combination of centrally mediated hypoventilation, and ventilate was improved and further mechanical pain and V/Q mismatch were the most likely cause for ventilation was deemed to be unnecessary. Nonsteroidal observed blood gas changes in this case. However, an anti-inflammatory medications and antimicrobials were increased A-a PO2 gradient is also seen in imbalances of administered pre- and post operatively. Diuresis was not reduced oxygen delivery (DO2) and increased oxygen deemed to be necessary. uptake (VO2) (Marino 2007). Conditions that reduce DO2 It is unclear as to what combination of pulmonary such as low cardiac output or anaemia, or increased VO2, contusion, pulmonary oedema, atelectasis or ALI/ARDS, due to hypermetabolism, were not apparent in this foal. caused the observed pulmonary compromise pre- and EQUINE VETERINARY EDUCATION / AE / april 2009 191

post operatively in this foal. This highlights the complex Groeneveld, J.A.B. (2007) Increased permeability-oedema and physiology of pulmonary damage. The rapid recovery atelectasis in pulmonary dysfunction after trauma and surgery: a prospective cohort study. BMC Anesthesiol. 7, 1-8. after surgery and the observation of arterial hypoxaemia Hance, S.R. and Robertson, J.T. (1992) Subcutaneous emphysema from responsive to treatment make ARDS less likely in this case. an axillary wound that resulted in pneumomediastinum and bilateral pneumothorax in a horse. J. Am. vet. med. Ass. 200, 1107-1110. Conclusion Hassel, D.M. (2007) Thoracic trauma in horses. Vet. Clin. N. Am.: Equine Pract. 23, 67-80. Post traumatic parenchymal lung injury is a common Jean, D., Laverty, S., Halley J., Hannigan, D. and Leveille R. (1999) complication in human trauma patients. There are no prior Thoracic trauma in newborn foals. Equine vet. 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