In the United States, each year, approximately 15,000 patients present to emergency services because of carbon monoxide (CO) poisoning, and approximately 500 of these patients die.1,2 Because the signs and symptoms of CO poisoning are relatively nonspecific, diagnosis is often very difficult. Thus, the true incidence of CO poisoning is unknown. The reported mortality rate ranges between 1% and 31%.3 The incidence and mortality rate in Turkey are unknown. CO poisoning constitutes a significant diagnosis in poisoning patients admitted to emergency departments and intensive care units (ICUs).4
Compartment syndrome because of CO poisoning is rarely seen. We present a case of CO poisoning in a patient who developed compartment syndrome in both thighs and the perineum as well as acute renal failure and systemic capillary leakage syndrome. Written informed consent was obtained from the patient to publish this report.
A 30-year-old man, found unconscious in a house heated by a brazier, was evaluated in an emergency department. His Glasgow Coma Score was 9 (best eye response, 2; best verbal response, 3; and best motor response, 4), 80/40 mm Hg arterial blood pressure, 36.7°C body temperature, and 90% carboxyhemoglobin level. The patient was tracheally intubated and transferred to an ICU. Positive pressure ventilation with 100% O2 resulted in a progressive decrease in the carboxyhemoglobin level to 43.3%.
The patient’s laboratory findings were as follows: 9 mg/dL prealbumin, 2089 U/L aspartate transaminase, 727 U/L alanine transaminase, 3.68 g/dL total protein, 1.91 g/dL albumin, 140 mg/dL urea, 6.5 mg/dL creatinine, 81,890 U/L creatinine kinase, 2610 U/L creatinine kinase-MB, 128 mmol/L sodium, 6.6 mg/L potassium, 96 mmol/L chloride, 4.5 mg/dL calcium, 132 lactate, 19.3 g/dL hemoglobin, and 53.8 hematocrit. Urinalysis documented a pH 5.5, density 1037, protein ++, bilirubin +, and hemoglobin +++. Dense erythrocytes were observed on microscopic evaluation. Therapeutic measures were instituted to correct the acid-base and fluid-electrolyte abnormalities. The initial increase in hematocrit level decreased rapidly despite the absence of a focus of bleeding. Blood smears showed widespread hemolysis. Twenty-four units of erythrocyte suspension and 27 units of fresh-frozen plasma were administered. By the third day of treatment, the patient displayed generalized body edema. On physical examination, both of the lower extremities were cold, pale, and very tense. Several of his toes developed cyanotic discoloration. Pulses could not be manually palpated from the tibialis posterior and dorsalis pedis arteries of both lower extremities nor could they be detected with Doppler ultrasonography. Compartment pressures were measured in the lower extremities and were found to be 47 mm Hg in the left thigh, 48 mm Hg in the left cruris, 43 mm Hg in the right thigh, and 45 mm Hg in the right cruris. Urgent fasciotomies were performed (Fig. 1). After performing the fasciotomies, the tibialis posterior and dorsalis pedis pulses became palpable.
The patient subsequently developed acute oliguric renal failure, and daily hemodialysis was initiated. By the 17th day in the ICU, muscle necrosis developed and débridement was necessary. The patient’s general condition improved, and he was admitted to the orthopedic ward on the 21st day in the ICU. The fasciotomies were ultimately closed, physical therapy was initiated, and the patient was finally discharged. At the most recent follow-up visit, no residual problems were observed except for mild stiffness in his knees.
CO is a colorless and odorless gas that is formed by incomplete burning of fossil fuels. Its normal concentration in the atmosphere is <0.001%. It is fatal when the level exceeds 0.1%.5 CO poisoning is reported to be one of the important causes of morbidity and mortality in many parts of the world.6
The amount of CO absorbed by the body depends on minute ventilation, exposure time, and CO concentration in the environment. CO has 200 times greater affinity to hemoglobin, myoglobin, and intracellular cytochrome oxidase than O2. Inspired CO rapidly diffuses from the alveolar–capillary interface, strongly binds to hemoglobin, and forms carboxyhemoglobin. Carboxyhemoglobin inhibits oxidative phosphorylation through cytochrome p-450, causes cellular anoxia, and reduces O2 delivery to tissues by sliding the oxyhemoglobin dissociation curve to the left. In this way, CO causes tissue hypoxia, anaerobic metabolism, and lactic acidosis.7–11
Because CO poisoning is nonspecific, it is sometimes confused with other maladies such as viral diseases. Nonspecific symptoms of CO poisoning are headache, vertigo, nausea, vomiting, confusion, visual problems, and palpitations. CO poisoning often affects many people at the same time. It may present with nausea and vomiting in infants and be incorrectly diagnosed as gastroenteritis.12–14 In young adults, CO poisoning commonly results in peripheral neuropathy, and these patients may develop ischemic muscle contractions because of muscle necroses.15
Rhabdomyolysis is a well-known complication of CO poisoning.16,17 Acute renal failure because of rhabdomyolysis caused by CO poisoning was first reported by Florkowski et al.18 The main reason tubular damage is associated with rhabdomyolysis is the presence of myoglobinuria. Myoglobinuria is present in 40% of patients with acute tubular necrosis.16–18 Our patient developed acute renal failure after severe acute tubular necrosis presenting with severe oliguria, low urinary osmolarity, low sodium, and high urea and creatinine concentrations requiring daily hemodialysis.
Our patient also developed systemic capillary leakage syndrome, which was first described by Clarkson et al.19 This syndrome causes hypotension, hypovolemia, hypoalbuminemia, hemoconcentration, generalized edema, renal damage characterized by paraproteinemia, and increased compartment pressures because of ischemic myonecrosis-induced rhabdomyolysis. In our case, systemic capillary leakage syndrome probably developed because of severe rhabdomyolysis.
Compartment syndrome is usually seen as a consequence of trauma such as fracture, soft tissue injury, crush syndrome, and blunt injury, and 75% of the patients have fractures. It usually develops in the perineum, hands, forearms, arms, shoulders, back, thighs, and legs. However, many cases of compartment syndrome have been reported in nontraumatic settings including ischemia–reperfusion events after arterial injury, exercise, prolonged limb compression, anticoagulation therapy, fluid infusion, snake bite, thrombosis, viral myositis, placement of orthopedic casts, circumferential dressing, burns, and bleeding disorder.20–23
Mubarak et al.24 defined compartment syndrome as a deficiency of blood supply at a microvascular level with possible myoneural damage because of interstitial pressure increases in an osteofascial compartment. When an acute compartment syndrome develops, urgent surgical decompression should be done to reestablish perfusion. If not treated urgently, functional loss and permanent extremity contracture because of nerve and muscle ischemia may result.20,22 Compartment syndrome in CO poisoning is a rare but well-known complication.6,25 In our case, we observed high levels of muscle enzymes because of degradation, myoglobinuria, and severe and widespread muscle necrosis. In our patient compartment, syndrome requiring urgent fasciotomy was present in both lower extremities (both legs and cruris). Compartment syndrome affecting the thigh is very rare in CO poisoning. To the best of our knowledge, there is only 1 report of compartment syndrome because of CO poisoning affecting >1 extremity.26
The initial treatment of patients with symptomatic CO poisoning is very simple. The most important thing in treatment is removing the patient from the environment with high CO as soon as possible and providing high inspired O2 concentrations. Providing 100% O2 with an airway may dramatically decrease the half-life of carboxyhemoglobin. With 100% O2 ventilation, CO is released from carboxyhemoglobin. These patients should be hospitalized with cardiac monitoring and close evaluation of fluid–electrolyte and acid-base balances.27–29 Hyperbaric O2 treatment may be helpful and is often not available in many hospitals.
In our case, the patient presented with an absence of a history of trauma and trauma symptoms (ecchymosis, deformity, hemorrhage, swelling, lacerations, abrasions, contusions, etc.). Radiographies of all the extremities were evaluated and were normal. Because the patient was found lying on his back and no lesions were found because of pressure on the affected extremities, we concluded that the development of compartment syndrome was not induced by pressure resulting from compression. We considered that this condition was possibly a direct effect of CO poisoning itself rather than being because of trauma and prolonged limb compression. High levels of CO trigger the formation of nonhemoglobin structures and free radicals and cause tissue ischemia and necrosis. This leads to increased capillary leaking, intramuscular hemorrhage, swelling, and widespread edema in subcutaneous tissues.
In addition, the O2 therapy that was applied using high inspired O2 concentrations might have increased this effect. There are studies supporting this hypothesis.25 Durán et al.30 reported that O2-derived free radicals could peroxidate the lipid component of cell membranes, leading to enhanced capillary permeability, causing compartment syndrome.
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