CLINICAL MANAGEMENT OF HAFF SYNDROME

• DOI: 10.22533/at.ed.1592182201044

• Palavras-chave: Haff Syndrome. Black Urine Disease. Rhabdomyolysis. Clinical Management.

• Keywords: Haff Syndrome. Black Urine Disease. Rhabdomyolysis. Clinical Management.

• Abstract:

  INTRODUCTION: Haff's disease was first reported in 1924 on the Baltic Sea coast. This syndrome is related to a toxin that is still unknown, but can be found in certain freshwater fish when they are contaminated. In the progression of this pathology, a condition called rhabdomyolysis was observed, an aggravating situation that, if not treated immediately, can lead to death. The diagnosis of Haff's disease is based on clinical suspicion, epidemiological history, and elevated levels of muscle necrosis markers. As it is a rare clinical syndrome, underdiagnosed, with an increase in incidence and with a good prognosis if treatment is indicated in a timely manner, this study aims to report what is known about the current clinical management of Haff Syndrome, focusing on greater clarification about of the disease. METHODOLOGY: This is a literature review in the Scielo, BVS and Google Scholar databases, in addition to the emergency book of the University of São Paulo for comparative purposes. Five articles were selected from 2005 to 2021, in Portuguese, correlated with different aspects of the theme. RESULTS: The approach is based on the prevention of acute tubular necrosis and the prompt recognition and correction of electrolyte and acid-base disturbances. In the first 24-48 hours, hydration with isotonic saline must be performed, about 1 to 2 L/h. After the start of diuresis, the volume replacement required is 100 to 200 mL/hour. To increase urinary output, 10g of mannitol and 40 mEq of sodium bicarbonate in 0.45% saline can be considered. If refractory oliguria is present, urgent hemodialysis is indicated. If hyperkalemia, evaluate the use of intravenous glucoinsulin, intravenous sodium bicarbonate, oral exchange resin or even furosemide. If refractory hyperkalemia, also indicate hemodialysis. For hyperphosphatemia, the oral chelator or aluminum hydroxide, avoiding calcium carbonate, are options. Hypocalcemia must only be corrected in symptomatic cases or in the presence of severe hyperkalemia. Allopurinol may be indicated to control hyperuricemia and also contribute to the elimination of free radicals. As for metabolic acidosis, correction of the other parameters tends to normalize it. If severe acidosis, as in the case of serum bicarbonate less than 15 mEq/L, the use of 50 mEq of intravenous sodium bicarbonate is an alternative. CONCLUSIONS: Since the disease-causing toxin has not yet been identified and the pathophysiology remains unclear, treatment involves general supportive measures in addition to specific interventions for complications.

• Número de páginas: 6