Article, Gastroenterology

Bacterial translocation in heat stroke

Case Report

Bacterial translocation in heat stroke Abstract

The scientific community is fully aware of the importance of heat-related illness and heat stroke syndrome. Numerous guidelines have been recently published and most of them agree on the key role played by the intestine. Likewise, the role of endotoxinemia in the pathophysiology is well established. However, the possibility of bacterial transloca- tion is not mentioned. Our patient illustrates the likelihood of bacterial translocation in heat stroke and consistently the potential need of antibiotic therapy. A 45-year-old man diagnosed with paranoid schizophrenia was confined in a penitentiary center. One summer day in which a temperature of 41?C was observed in the shade, the patient was found in deep coma with an axillary temperature of 42?C. multiorgan failure was detected in the hospital. Other causes of coma and/or hyperthermia were excluded, and heat stroke was diagnosed. Blood cultures were positive for Pseudomonas aeruginosa and Escherichia coli. Infection site was not identified despite of an exhaustive search. The patient fully recovered after 48 hours. On the basis of review of the literature, we think that bacterial translocation can take part in the pathophysiology of heat stroke. Therefore, antibiotic treatment must be evaluated in heat stroke patients.

heat stroke is a condition of complex pathogenesis in which the intestine appears to play a key role [1]. The intestinal lesion produced in HS has both chemical and physical consequences, as mucosa disruption permits bacterial translo- cation in the form of either endotoxinemia or bacteremia [2]. However, despite potential bacterial participation in HS, antibiotic therapy is not considered in guidelines [3].

We describe the case of a 45-year-old man diagnosed with paranoid schizophrenia in residual phase on therapy with risperidone, levopromazine, and biperiden confined in a mental hospital. As a result of his mental condition, the patient maintained continuous, low-intensity physical activity.

On the day of admission, a temperature of 41?C in the shade and relative humidity of 78% were observed. The patient was found in a deep coma, with a blood pressure of 70/40 mm Hg and axillary temperature of 42?C. At hospital admission, the patient’s Glasgow score was 3 points and he exhibited flaccid

tetraplegia. Blood pressure was 90/50 mm Hg and temperature was 41?C. The Laboratory workup showed the following: leukocytes 8900/mm3 (80% polymorphonuclear), hemoglobin 12 g/dL, platelets 16 000/mm3), glucose 108 mg/dL, sodium 127 mEq/L, potassium 2.7 mEq/L, Creatine phosphokinase 25 000 U/L, Quick index 39%, fibrinogen 80 mg/dL, activated partial thromboplastin time 48 seconds, and D-dimer 895 mg/ dL. The chest x-ray was normal.

The patient was intubated and connected to mechanical ventilation to preserve the airway. Physical measures were instituted, and the temperature dropped to 37.5?C in less than 5 hours. The Cerebrospinal fluid analysis was normal. A Swan Ganz catheter was introduced, disclosing the presence of hyperdynamic shock. Once the endovascular volume was corrected, dopamine perfusion was necessary. Blood and Urine samples were drawn and cultured, and meropenem and levofloxacin therapy were initiated. Pseudomonas aerugi- nosa and Escherichia coli were isolated in the blood cultures and found to be susceptible to the prescribed treatment.

Abdominal ultrasound, cerebral and thoracic-abdomino- pelvic computed tomography, and transesophageal echocar- diography showed no abnormalities. After 48 hours, cardiovascular, renal, and hematologic function was normal. The Weather conditions combined with our patient’s continuous physical activity and the use of neuroleptic agents led to the onset of HS. The absence of muscle stiffness and the rapid control of hyperthermia make a diagnosis of neuroleptic malignant syndrome improbable. The clinical symptoms are consistent with HS, and the examinations

revealed no other conditions.

Although coincidence of HS and bacteremia is possible, our opinion is that bacteremia was secondary to intestinal translocation in the context of HS. Structural lesions of the Intestinal mucosa have been seen in numerous cases of HS as well as in autopsies of burn patients [1,4]. The disruption of intestinal mucosa would allow bacterial components or complete microorganisms to enter the bloodstream [1]. This possibility appears to be confirmed by studies that analyze the behavior of serum procalcitonin in patients with HS [5,6]. The systematic increase of serum procalcitonin indicates the coexistence of an infectious process that is not readily identifiable. The role of the intestinal flora in the pathogenesis of HS has also been studied in animal models in which the use of digestive decontamination achieved a lower mortality [7].

0735-6757/$ – see front matter (C) 2009

1168.e2 Case Report

The proposed hypothesis would require a prospective study. However, we consider it advisable to evaluate antibiotic therapy when managing patients with HS.

Paula Ramirez Veronica Marti

Alberto Marquez de la Plata

Gema Salinas Juan Bonastre Miguel Ruano Intensive Care Unit

Hospital Universitario la Fe 46009 Valencia, Spain

E-mail address: [email protected] doi:10.1016/j.ajem.2008.11.025


  1. Hall DM, Buettner GR, Oberley LW. Mechanisms of circulatory intestinal barrier dysfunction during whole body hyperthermia. Am J Physiol Heart Circ Physiol 2001;280:H509-21.
  2. Graber CD. Fatal heat stroke. Circulating endotoxin and gram-negative sepsis as complications of heat stroke. JAMA 1971;216:1195-6.
  3. Bouchama A, Knochel JP. Heat stroke. N Engl J Med 2002;346:1978-88.
  4. Law EJ, Day SB, MacMillan BG. Autopsy findings in the upper gastrointestinal tract of 81 burn patients. A review. Arch Surg 1971;102: 412-5.
  5. Nylen ES, Al Arifi A, Becker KL. Effect of classic heatstroke on serum procalcitonin. Crit Care Med 1997;25:1362-5.
  6. Hausfater P, Hurtado M, Sebastian P, et al. Is procalcitonin a marker of critical illness in heatstroke? Intensive Care Med 2008;34: 1377-83.
  7. Bynum G, Brown J, Dubose D. Increased survival in experimental dog heatstroke after reduction of flora. Aviat Space Environ Med 1979;50: 816-9.