The Journal of Maharashtra Orthopaedic Association September / December - 2006 Fat Embolism Syndrome And Crush Syndrome
Dr. Shivaprasad D. Khot M.S. Orth., D. Orth. ( Mumbai)
Dr. Rahul S. Khot M.B.B.S., D. Orth., D.N.B.
v Introduction v v Causes v Fat Embolism syndrome is a major cause of FES occurs most commonly as an early morbidity and mortality after multiple long bone complication of fractures of the pelvis and long fractures and is an important cause of ARDS. bones. FES is also reported in other entities: FES may be defined as, “a complex alteration l As a complication of reaming of medullary of homeostasis that occurs as an infrequent canals of long bones complication of fractures of long bones and pelvis l As a complication of reaming and cementation and manifests clinically as acute respiratory during joint replacement ? Massive soft tissue insufficiency”. injury ? Severe burns FES develops when fat emboli become l Liposuction impacted in pulmonary microcirculation and other l Chronic osteomyelitis microvascular beds such as the brain and is l Metabolic disorders characterized by respiratory failure, cerebral l dysfunction and petechiae. In-patients with pre Neoplasms existing pulmonary disease the addition of FES can l Renal transplant be life threatening. FES is an a important cause of l Bone infarcts in hemoglobinopathoies acute respiratory distress syndrome. With prompt l Collagen disease recognition, the treatment of the fat embolism l syndrome has become more specific and less empiric, Diabetes resulting in decrease morbidity and mortality. In l Severe infection recent years prevention of fat embolism syndrome l Inhalation anesthesia by early fracture fixation and patient mobilization l Blood transfusion has become the focus of a wave of clinical v Historical Aspects v investigation. Acute respiratory insufficiency after skeletal FES is a well-known entity as a complication of long bone fractures from one and half centuries. trauma has multiple causes : Zenker in 1861 described fat droplets in the l Fat embolism lung capillaries of a rail-road worker with fatal l Aspiration of gastric contents thoraco-abdominal crush injury. l Pulmonary edema Wagner in 1865 described the pathologic l Airway obstruction features of fat embolism. l Pneumonia Von Bergmann in 1873 was the first to establish FES in a patient with femoral fractures by l Pulmonary contusions postmortem demonstration of a large amount of l Shock lung pulmonary fat.
Vol. 5 / 6 - Year 2 - Sept. / Dec. 2006 209 Czerny in 1875 described the symptoms of others proposed a biochemical theory which FES and the importance of fundoscopic examination incriminates free fatty acids. in its diagnosis. According to them, local hydrolysis of Fenger and Salisbury in 1879 made the first triglycerides and neutral fat emboli by pneumocyte clinical diagnosis of FES in a patient with femoral lipase results in increased free fatty acids. fractures and confirmed it by demonstrating massive v Free fatty acids have been shown to be toxic fat emboli in the lung at autopsy. to lung parenchyma and lead to v Incidence v l Disruption of alveolar capillary membrane The exact incidence of FES is not known. The l Decreased surfactant production clinical signs and symptoms develop in 0.5% to 2% l Interstitial hemorrhage and of patients with long bone fractures and in 10% of patients with multiple fractures. The risk of FES l Pulmonary edema resulting in pulmonary increases with the increased incidence of multiple dysfunction. fractures in major automobile accidents. FES is rare Thus, the latent period before clinical in children probably because of low fat content in manifestations appear may be explained by the time their marrow. needed for lipoprotein lipase to convert neutral fat v Pathogenesis And Pathophysiology v to toxic free fatty acids. v Clinical Presentation v This is a subject of conjecture and controversy. The source of embolic fat is thought by most to be Onset of symptoms is usually within 12 to 72 the bone marrow. Bone marrow elements have been hours but may manifest as early as 6 hours and as demonstrated in lung sections, indicating that late as 10 days. mechanical fat embolization does occur. Two Arterial hypoxemia is the hallmark of FES and theories have been offered for the pathogenesis of the clinical manifestations are a result of reduced FES: blood flow to the lungs and brain (a) Mechanical theory : This classic theory Early symptoms are : postulates that triglyceride particles from injured fat l Shortness of breath marrow enter the circulation and obstruct the pulmonary micro vessels. Fat globules vary in size l Restlessness from 2 to 200 microns and most get lodged in vessels l Confusion less than 75 microns in diameter. The classic triad of FES involves : v The blockage of pulmonary capillaries l Pulmonary dysfunction results in : l Cerebral dysfunction and l Venoarterial shunting l Cutaneous changes. l Hypoxemia and Pulmonary Dysfunction l Alveolar hypoperfusion leading to pulmonary dysfunction. Features of pulmonary insufficiency are the earliest signs of FES and include : (B) Biochemical Theory : As FES has also l been documented in non traumatic disorders, the Tachypnoea with respiratory rate more than mechanical theory cannot adequately explain the 30 per minute phenomenon. Alternative or additional mechanisms l Dyspnoea have therefore been suggested. Peltier, Barie and l Cyanosis
Vol. 5 / 6 - Year 2 - Sept. / Dec. 2006 210 l Rales and rhonchi Sevitt classified FES into 3 distinguishable clinical l Respiratory failure and ARDS presentations : l l Occasionally hemoptysis and pulmonary Sub clinical FES edema l Non fulminant FES l Cerebral Dysfunction Fulminant FES Features include : Sub clinical FES l Restlessness l Probably occurs in almost all long bone fractures of the lower extremity and fractures l Confusion and disorientation of the pelvis l Irritability and delirium l Characterised by decreased PaO2, decreased l Stupor and coma Hb% and decreased platelets. No clinical l Convulsions signs and symptoms of respiratory insufficiency. l Diffuse neurological deficit. The neurological features in FES appear to Non-fulminant FES change periodically and may sometimes progress l Clinical signs and symptoms are clearly very rapidly. evident. l Cutaneous Changes Respiratory insufficiency, cerebral symptoms and petechiae appear classically Are characterized by : l Typical radiological and haematological l Petechiael rashes located in the upper anterior changes can be detected chest, axilla, neck, oral mucous membrane and conjunctiva. Fulminant FES l Appear on the second to third day l Rarer form and appears within hours of injury l May occur periodically with accompanying l Characterised by severe respiratory failure and attacks of coma altered mental status and convulsions. l Resolve within 7 days FES should be Strongly Suspected if the Patient The distribution of petechiae is theorized to has the related fat particles floating in the aortic arch l Unexplained Dyspnoea and Tachycardia and embolising to non-depended skin areas via l Unexplained confusion and cerebral subclavian and carotid arteries. dysfunction The other signs of FES include : l Petechiae in the upper half of the body. l Pyrexia : Fracture fever / haematoma fever Often the signs and symptoms may be masked l Tachycardia: pulse rate more than 140 per by shock, coma, head injury and anesthetic drugs. minute v Diagnosis v l Retinal changes which include edema, The diagnosis of FES is essentially by clinical hemorrhage or intravascular fat globules as features and there are no pathognomonic tests for seen on fundoscopy confirmation. However certain laboratory and x-ray l Renal changes like lipuria features aid in the diagnosis of FES. l Hepatic changes like jaundice Laboratory Investigations l Urinary incontinence l Sustained reduction in PaO2 levels (partial
Vol. 5 / 6 - Year 2 - Sept. / Dec. 2006 211 pressure of oxygen in arterial blood) below w Cerebral dysfunction w Tachycardia 60 mm of Hg as detected by arterial blood gas w Petechiael rash w Retinal changes analysis indicates FES. Serial determination of PaO2 levels is necessary. Clinical features w Jaundice appear only when the levels fall below 65 mm w Renal changes of Hg. l Thrombocytopenia; platelets below 150000 Laboratory Features (at least one) cell per cubic millimeter is commonly seen. w Fat macroglobulinemia l Detection of fat globules in urine, sputum, w Anemia CSF and blood; usually difficult to do. Gurd w Thrombocytopenia suggested detection of pathological fat in filtered venous blood. Cryostat frozen section w High ESR of clotted blood may reveal fat globules. They proposed that if any one major and four l Biopsy of petechiael skin lesions may reveal minor features are present after a latent period after presence of fat. injury, then a diagnosis of FES could be made. l Elevated serum lipase and free fatty acid levels Schonfeld et al proposed a quantitative means l Broncho alveolar lavage and detection of fat of diagnosing FES droplets within cells recovered by lavage may v Schonfelds Fat Embolism Index v aid in rapid diagnosis of FES. v ECG v Symptoms Score Show only non-specific changes like T wave w Petechiae 5 inversion, prominent S waves and occasional w Diffuse alveolar infiltrates 4 arrhythmias. w Hypoxemia (PaO2 less than 9.3 kPa) 3 X-ray w Confusion 1 Chest X-ray reveals a diffuse fluffy bilateral w Fever (more than 38’C) 1 infiltrate classically called “snow storm” appearance. w Tachycardia 1 This may progress to widespread airspace (more than 120 beats per min) consolidation caused by alveolar hemorrhage and edema. w Tachypnea (more than 30 per min) 1 A differential diagnosis of cardiogenic edema A cumulative score greater than 5 is necessary and traumatic lung contusion must be kept in mind. for a positive diagnosis of FES. Since there are no definitive and pathogn- v Differential Diagnosis v omonic features of FES, several authors have Since FES involves respiratory insufficiency suggested some aids in diagnosing FES. and cerebral dysfunctions other conditions causing Gurd and Wilson have divided the features of the same features should be kept in mind. FES into major and minor criteria. The Respiratory Insufficiency Should be v Gurds Criteria v Differentiated From Major Features Minor Features l Pulmonary contusion (at least one) (at least four) l Pulmonary embolism w Respiratory w Pyrexia l insufficiency Bronchial pneumonia
Vol. 5 / 6 - Year 2 - Sept. / Dec. 2006 212 Radiological Features Differentiating FES From Traumatic Lung Contusion are Features FES Lung Contusion
w Onset of X-ray changes after trauma. 1 to 2 days Immediate w Distribution Bilaterally symmetrical Unilateral or asymmetrical
Cerebral Dysfunction Should be Differentiated From l Subdural or extradural haematoma l Cerebral contusion. l Diabetic coma
Clinical Features Differentiating Cerebral Fat Embolism From Craniocerebral Trauma Symptoms and Signs Cerebral FES Craniocerebral Trauma w Lucid interval 48 to 72 hours 6 to 10 hours w Confusion Severe Moderate w Pulse rate Rapid more than 140/min Slow w Onset of coma Rapid Slow w Localising signs Usually absent Usually present w Decerebrate rigidity Early Terminal
v Treatment v The treatment of FES consists of general measures and specific measures
General Measures Include l Maintenance of airway. l Maintenance of fluid and electrolyte balance. l Blood transfusion. l Immobilization of fractures in splints / POP to prevent further emboilization ?J* Analgesics and when indicated antibiotics. l Monitoring of BP, urinary output, PaO2.
Specific Measures Respiratory Support is the Mandatory in the Management of FES l Oxygen therapy via mask / nasal cannula to maintain PaO2 at 90 mm of Hg ?> Endotracheal intubation and mechanical ventilation if respiratory distress is impending l Corticosteroids; methyl prednesolone 10 mgs/kg/daily in 3 divided doses i.v. should be administered. It helps by; w Inhibiting the inflammatory response of the lungs to emboli w Limiting the decrease in PaO2
Vol. 5 / 6 - Year 2 - Sept. / Dec. 2006 213 l Ethanol / alcohol: accidental evidence shows recognition and aggressive treatment for the patient those intoxicated patients fare better after to recover. Mortality is still close to 5% to 15% and multiple fractures and FES. It has been is closely related to severity of respiratory suggested that a bolus of alcohol may prevent dysfunction. Morbidity is usually secondary to focal and limit the effects of FES probably by acting cerebral neurological deficit. as a lipase inhibitor. Intramedullary Reaming and FES l Other agents like heparin and hypertonic l Reaming of the medullary canal prior to glucose etc. have been tried with no insertion of a nail or a prosthesis is know to measurable success. increase the incidence of FES. Fracture Stabilization l Insertion of femoral stem during hip It has been shown by many authors that early replacement increases the intramedullary fracture fixation by unreamed intramedullary nailing pressure and may lead to embolisation of fat considerably reduces the incidence of FES. Early particles and bone marrow leading to FES. internal fixation of fractures aids by, l In these instances not only fat particles but l Allows the patient to be upright and thus other substances like tissue particles, improves lung function thromboplastin, fibrin degradation products l Decompresses the fracture haematoma and etc may be the culprits thus eliminates source of emboli l It is therefore wise to use unreamed nails in l Eliminates pain and stress of motion at patients with multiple injuries. fracture site and reduces need for opiate v Summary v analgesics l Fat embolism, usually sub clinical occurs in Prophylaxis of FES the majority of patients with fractures of pelvis and long bones. We have all been taught that prevention is better than cure. The various measures we can take l Respiratory insufficiency, cerebral dysfun- to prevent FES in an injured patient are, ction and petechiae appearing 48-72 hrs after multiple fractures are considered pathgno- l Gentle handling, proper splinting and careful monic of fat embolism. transport of the patient with multiple injuries. l Despite certain laboratory and radiological l Aggressive treatment of hypovolemic shock diagnostic aids, clinical features are still the l Early stabilization of fractures corner stone for diagnosis of fat embolism. l Reduce bone marrow release into circulation l Treatment consists of respiratory support, during preparation of medullary canal for volume replacement, cortico-steroid intramedullary nailing / prosthesis insertion. therapy and possible fracture fixation. l Identification of patients at risk by regular l Early detection, careful monitoring and monitoring with pulseoximetry, blood gas aggressive therapy have considerably reduced analysis etc. the morbidity and mortality due to fat v Prognosis v embolism. FES in its subclinical form is self-limiting and l In spite of all available therapy, fulminant fat recovery is almost complete. FES in its non- embolism with severe respirator}’ failure can fulminant and fulminant forms needs early still be fatal.
Vol. 5 / 6 - Year 2 - Sept. / Dec. 2006 214 v Crush Syndrome v
The term crush syndrome, or traumatic Fluid shift produces shock rhabdomyolysis, refers to the sequela of prolonged (extensive amount of muscle involved) continuous pressure on muscle tissue. Crush syndrome refers to the systemic manifestation associated with crush injuries, such as hyperkalemia, Release of potassium, phosphorus, lactic acid Myoglobinemia and anuric renal failure. and myoglobin circulation v Causes v Cardiac arrest, shock, acidosis and renal failure. Commonly Seen in Clinical Features v l Earth quake victims v l Bombings Local Features l Train accidents l Edema with or without cellulitis l Motor vehicle accidents l Hematoam with or without abscess l Prolonged application of military anti shock l Copartment syndrome due to extensive muscle trousers edema v Pathophisiology v Systemic Complication Increased intramuscular pressure - l Hypovalemia more than 240 mm / hg l Anemia l Hypotention Muscle break down (direct pressure) l Tachycardia l Electrolyte abnormalities like . Ischemia and necrosis of muscles (independently) w Hyperkalemia w Hypocalcemia Reperfusion of ischemic necrotic muscle w Phosphorus and magnesium imbalance with oxygenated blood w Coagulopathy w Renal failure (5-15%) Reperfusion myopathy (second insult) v Investigation v
Forms reactive oxygen metabolites. l Hematocrit l K,Na,Ca,P
Xanthine oxidase + hypoxanthine + molecular l Platelet Count oxygen releases in skeletal muscle l Blood urea l Serum creatanine Rapid production of super oxide radicals l CPK and hydrogen peroxide l Urine for pigment l Blood gases Failure of ion pumps and increased membrane l Appropriate radiographs permeability of myocytes and micro vasculature
Vol. 5 / 6 - Year 2 - Sept. / Dec. 2006 215 v Treatment v l Correct electrolyte imbalance. The treatment of crush syndrome is divided l Renal dialysis required if anuria persist in to systemic treatment and local treatment. Local Treatment Systemic Treatment The optimal approach to the local injury is Begins with in an hour or immediately still a matter of debate. Most authors recommended after rescue. Treatment should begin immediately conservative management unless until there is by anticipating the onset of this syndrome. threatening compartment syndrome. l Aggressive fluid resuscitation is the mainstay Fasciotomy is the treatment of choice In case of treatment. of severe crush injury wound debridement and 1500 ml / hour crystalloid saline infusion in exploration can be done. adults to maintain a urine out put of at least Reference 100 ml / hour. Rock wood and green l Administer 1 gr/k.g. Mannitol and 100 mEq Pubmed bicarbonate in order to increase diuresis, Medline which interns increases the excretion of urine and prevents renal failure. ❃ ❃ ❃ l Administration of Allopurinol limits reperfusion by inhibiting xanthine oxidase activity.
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