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BUFFALO FISH POISONING

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Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) Ingestion of buffalo fish (Ictiobus cyprinellus), which have presumably ingested fat-soluble toxins while feeding on blue-green algae, may result in a food poisoning. The toxin appears to be heat stable, based on case reports in which the fish were thoroughly cooked prior to ingestion. Haff disease, a syndrome of unexplained rhabdomyolysis, has resulted from this food poisoning.

Specific Substances

    A) POISONING, BUFFALO FISH
    1) Fish poisoning, buffalo
    2) Haff disease
    BIGMOUTH BUFFALO
    1) Common Buffalo
    2) Gourdhead Buffalo
    3) Redmouth Buffalo Fish
    4) Stubnose Buffalo
    5) Mud Buffalo
    6) Lake Buffalo
    7) Slough Buffalo
    8) Scientific name: Ictiobus cyprinellus
    BUFFALO SMALLMOUTH
    1) Blue Pancake
    2) Brown Buffalo
    3) Suckermouth Buffalo
    4) Rooter
    5) Razorback
    6) Quillback Buffalo
    7) Carp
    8) Humpedback Buffalo
    9) Liner
    10) Roachback
    11) Scientific name: Ictiobus bubalus
    QUILLBACK
    1) Carpsucker
    2) American Carp
    3) Silver Carp
    4) Eastern Carpsucker
    5) Plains Carpsucker
    6) Scientific name: Carpiodes cyprinus
    OTHER TYPES OF FISH IMPLICATED
    1) Crawfish
    2) Salmon
    3) Pacu (silver dollar fish)
    4) Tambaqui (black-finned colossoma)
    5) Pirapitinga (freshwater pompano)
    6) Freshwater pomfret (Colossoma brachypomum)
    7) Silver dollar fish (Mylossoma duriventre)

Overview

Life Support

    A) This overview assumes that basic life support measures have been instituted.

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) USES: Buffalo fish are used as a food source, and are endemic to the Mississippi river and its tributaries. The syndrome of rhabdomyolysis developing within 24 hours of fish consumption has been reported with other fish species and is also known as Haff disease.
    B) TOXICOLOGY: The chemical and pharmacologic properties of the buffalo fish toxin are unknown. It has been postulated that the toxin may originate in fat-soluble toxins present in blue-green algae that the fish eat, but this has not yet been confirmed. The toxin appears to be heat stable.
    C) EPIDEMIOLOGY: Toxicity is rare. Cases of buffalo fish poisoning have been reported in areas of Missouri, Texas, and California. Several cases have been reported in the former Soviet Union and Sweden. Consumption of salmon, crayfish, carp, Mylossoma and Collosoma species in Brazil, and freshwater pompano and pomfret have rarely been associated with a similar syndrome.
    D) WITH POISONING/EXPOSURE
    1) MILD TO MODERATE POISONING: Buffalo fish poisoning is characterized by a syndrome of rhabdomyolysis with severe generalized muscle pain and tenderness with weakness, especially in the lower extremities. Nausea and vomiting are common. Diaphoresis, tachycardia, bradycardia, hypertension, dyspnea, chest pain, and hypothermia may occur. Urine may turn brown-black or red. Elevations in liver enzymes and renal insufficiency may develop. ECG changes have been noted, including diffuse ST-segment changes. Electrolyte disturbances may occur.
    2) ONSET: Symptoms of muscle stiffness, muscle tenderness, and muscle rigidity usually occur 6 to 24 hours after eating contaminated food, although vomiting may occur as soon as 30 minutes after ingestion.
    3) DURATION: Symptoms generally resolve in 2 to 3 days.
    4) SEVERE POISONING: Severe rhabdomyolysis, tachypnea, respiratory insufficiency, acidosis, renal failure, and disseminated intravascular coagulation can occur with severe poisoning.
    0.2.3) VITAL SIGNS
    A) WITH POISONING/EXPOSURE
    1) Tachypnea, tachycardia, bradycardia, hypertension, and hypothermia have been reported.

Laboratory Monitoring

    A) Monitor serial serum creatine kinase, electrolytes, and renal function tests. Monitor liver enzymes, CBC, and INR in patients with severe toxicity.
    B) Obtain an ECG in symptomatic patients.
    C) Frequent monitoring of vital signs and support of vital functions (pulse, blood pressure, and respirations) may be required.
    D) Monitor oxygenation in symptomatic patients.
    E) Monitor urinalysis and urine output.

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) MANAGEMENT OF TOXICITY
    1) Initial treatment of rhabdomyolysis should be directed towards controlling acute metabolic disturbances such as hyperkalemia and hypovolemia. Administer sufficient 0.9% saline to maintain urine output of 2 to 3 mL/kg/hour. Monitor urine output, serum electrolytes, creatine kinase, and renal function. Early aggressive fluid replacement is the mainstay of therapy and may help prevent renal insufficiency. Administer inhaled beta adrenergic agonists if bronchospasm develops. Administer benzodiazepines as needed for agitation, muscle contractions, and muscle rigidity.
    B) DECONTAMINATION
    1) The role of gastric decontamination in buffalo fish poisoning is unknown. Although vomiting may occur soon after ingestion, many patients may not present until 6 to 24 hours after ingestion, making gastrointestinal decontamination of questionable benefit.
    C) AIRWAY MANAGEMENT
    1) Endotracheal intubation should be performed in patients who develop respiratory insufficiency secondary to muscle weakness or who are unable to protect their own airway.
    D) ANTIDOTE
    1) None
    E) INFECTIOUS DISEASE NOTIFICATION
    1) All cases of buffalo fish poisoning should be reported to the state health departments who in turn are requested to report to the Foodborne and Diarrheal Diseases Branch, Division of Bacterial and Mycotic Diseases, National Center for Infectious Diseases, CDC. Telephone: 404-639-2206.
    F) ENHANCED ELIMINATION
    1) No studies have addressed the utilization of extracorporeal elimination techniques in poisoning with this agent. However, hemodialysis may be considered in cases of severe renal failure due to buffalo fish toxins.
    G) PATIENT DISPOSITION
    1) HOME CRITERIA: Patients who are asymptomatic after consumption of buffalo fish may be monitored at home.
    2) OBSERVATION CRITERIA: Symptomatic patients should be referred to a healthcare facility for evaluation and treatment. Patients should be observed in a medical facility until CK is declining and signs and symptoms of toxicity are improved.
    3) ADMISSION CRITERIA: Patients with significant rhabdomyolysis, persistent vomiting, or other systemic effects should be admitted.
    4) CONSULT CRITERIA: Consult a medical toxicologist for assistance with medical management in patients who develop significant toxicity or in whom the diagnosis is unclear. Notify your local health department of suspected cases.
    H) TOXICOKINETICS
    1) ONSET: Symptoms of muscle stiffness, muscle tenderness, and muscle rigidity usually occur 6 to 24 hours after eating contaminated food, although vomiting may occur as soon as 30 minutes after ingestion. DURATION: Symptoms generally resolve in 2 to 3 days.
    I) DIFFERENTIAL DIAGNOSIS
    1) Includes other agents that may cause rhabdomyolysis.

Range Of Toxicity

    A) TOXICITY: Severity of illness may be related to the amount of toxin ingested. It is not known whether toxicity is dependent on the size of the fish.

Clinical Effects

Summary Of Exposure

    A) USES: Buffalo fish are used as a food source, and are endemic to the Mississippi river and its tributaries. The syndrome of rhabdomyolysis developing within 24 hours of fish consumption has been reported with other fish species and is also known as Haff disease.
    B) TOXICOLOGY: The chemical and pharmacologic properties of the buffalo fish toxin are unknown. It has been postulated that the toxin may originate in fat-soluble toxins present in blue-green algae that the fish eat, but this has not yet been confirmed. The toxin appears to be heat stable.
    C) EPIDEMIOLOGY: Toxicity is rare. Cases of buffalo fish poisoning have been reported in areas of Missouri, Texas, and California. Several cases have been reported in the former Soviet Union and Sweden. Consumption of salmon, crayfish, carp, Mylossoma and Collosoma species in Brazil, and freshwater pompano and pomfret have rarely been associated with a similar syndrome.
    D) WITH POISONING/EXPOSURE
    1) MILD TO MODERATE POISONING: Buffalo fish poisoning is characterized by a syndrome of rhabdomyolysis with severe generalized muscle pain and tenderness with weakness, especially in the lower extremities. Nausea and vomiting are common. Diaphoresis, tachycardia, bradycardia, hypertension, dyspnea, chest pain, and hypothermia may occur. Urine may turn brown-black or red. Elevations in liver enzymes and renal insufficiency may develop. ECG changes have been noted, including diffuse ST-segment changes. Electrolyte disturbances may occur.
    2) ONSET: Symptoms of muscle stiffness, muscle tenderness, and muscle rigidity usually occur 6 to 24 hours after eating contaminated food, although vomiting may occur as soon as 30 minutes after ingestion.
    3) DURATION: Symptoms generally resolve in 2 to 3 days.
    4) SEVERE POISONING: Severe rhabdomyolysis, tachypnea, respiratory insufficiency, acidosis, renal failure, and disseminated intravascular coagulation can occur with severe poisoning.

Vital Signs

    3.3.1) SUMMARY
    A) WITH POISONING/EXPOSURE
    1) Tachypnea, tachycardia, bradycardia, hypertension, and hypothermia have been reported.
    3.3.2) RESPIRATIONS
    A) WITH POISONING/EXPOSURE
    1) Hyperventilation may occur as a result of buffalo fish poisoning (Solomon, 1990).
    3.3.3) TEMPERATURE
    A) WITH POISONING/EXPOSURE
    1) Hypothermia may occur during buffalo fish poisoning (Burns et al, 2000; Solomon, 1990).
    3.3.4) BLOOD PRESSURE
    A) WITH POISONING/EXPOSURE
    1) Hypertension has been reported following Buffalo fish poisoning (Burns et al, 2000; Solomon, 1990).
    3.3.5) PULSE
    A) WITH POISONING/EXPOSURE
    1) Bradycardia (without hemodynamic compromise) has been reported following Buffalo fish poisoning (Burns et al, 2000).
    2) Tachycardia has also been reported following Buffalo fish poisoning.

Cardiovascular

    3.5.2) CLINICAL EFFECTS
    A) HYPERTENSIVE EPISODE
    1) WITH POISONING/EXPOSURE
    a) Hypertension has been reported following ingestion of buffalo fish (Burns et al, 2000; Solomon, 1990).
    B) ELECTROCARDIOGRAM ABNORMAL
    1) WITH POISONING/EXPOSURE
    a) Electrocardiographic changes, including diffuse S-T segment changes, have been reported as a result of buffalo fish poisoning (Solomon, 1990).
    C) CHEST PAIN
    1) WITH POISONING/EXPOSURE
    a) Chest pain has occurred in several cases following ingestion of buffalo fish (CDC, 1998) and crawfish (Diaz, 2015; Zhang et al, 2012; Krishna & Wood, 2001).
    b) INCIDENCE: In a series of 27 Brazilian patients with Haff disease, 19 (70%) developed chest pain (dos Santos et al, 2009).
    c) In a series of confirmed Haff disease cases reported in China from 1997 to 2014, chest pain occurred in 5 of 54 patients following consumption of freshwater pomfret (Colossoma brachypomum) (Diaz, 2015).
    D) BRADYCARDIA
    1) WITH POISONING/EXPOSURE
    a) Bradycardia (without hemodynamic compromise) has been reported following Buffalo fish poisoning (Burns et al, 2000).
    E) TACHYARRHYTHMIA
    1) WITH POISONING/EXPOSURE
    a) Tachycardia has been reported following Buffalo fish poisoning.

Respiratory

    3.6.2) CLINICAL EFFECTS
    A) HYPERVENTILATION
    1) WITH POISONING/EXPOSURE
    a) Tachypnea has been reported following buffalo fish poisoning (Solomon, 1990).
    B) DYSPNEA
    1) WITH POISONING/EXPOSURE
    a) Dyspnea has been reported following ingestion of crawfish (Diaz, 2015; Zhang et al, 2012; Krishna & Wood, 2001).
    C) EPIGLOTTITIS
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT: An 18-month-old child developed severe epiglottic enlargement and respiratory distress after a single bite of buffalo fish. The child's condition improved after administration of oxygen and epinephrine. An x-ray revealed an enlarged epiglottis and aryepiglottic folds. According to the authors, the reaction was likely due to scombroid fish poisoning but may have been anaphylactic (Herman & McAlister, 1991).
    D) RESPIRATORY FAILURE
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT: A 66-year-old man developed respiratory insufficiency secondary to severe muscle pain and weakness after eating a dish containing ground carp and buffalo fish. The patient required assisted ventilation but recovered (CDC, 1998).

Neurologic

    3.7.2) CLINICAL EFFECTS
    A) DYSESTHESIA
    1) WITH POISONING/EXPOSURE
    a) INCIDENCE: In a series of 27 Brazilian patients with Haff disease, 12 (44%) reported pain with light touch (dos Santos et al, 2009).
    B) DIZZINESS
    1) WITH POISONING/EXPOSURE
    a) In a series of confirmed Haff disease cases reported in China from 1997 to 2014, dizziness occurred in 18 of 54 patients following consumption of freshwater pomfret (Colossoma brachypomum) (Diaz, 2015).
    C) HEADACHE
    1) WITH POISONING/EXPOSURE
    a) In a series of confirmed Haff disease cases reported in China from 1997 to 2014, headache occurred in 12 of 54 patients following consumption of freshwater pomfret (Colossoma brachypomum) (Diaz, 2015).
    D) ALLODYNIA
    1) WITH POISONING/EXPOSURE
    a) Allodynia (pain on light touch) has been reported in several cases of confirmed Haff disease following ingestion of buffalo fish, boiled crayfish, and freshwater pomfret (Colossoma brachypomum) (Diaz, 2015).

Gastrointestinal

    3.8.2) CLINICAL EFFECTS
    A) NAUSEA AND VOMITING
    1) WITH POISONING/EXPOSURE
    a) Nausea and vomiting have been reported in several cases of Buffalo fish poisoning (Diaz, 2015; Burns et al, 2000; CDC, 1998) and following ingestion of crawfish (Diaz, 2015; Krishna & Wood, 2001).
    b) INCIDENCE: In a series of 27 Brazilian patients with Haff disease, 11 (41%) developed nausea and 9 (33%) vomited (dos Santos et al, 2009).
    c) In a series of confirmed Haff disease cases reported in China from 1997 to 2014, nausea with or without vomiting occurred in 34 of 54 patients following consumption of freshwater pomfret (Colossoma brachypomum) (Diaz, 2015).
    B) ABDOMINAL PAIN
    1) WITH POISONING/EXPOSURE
    a) Stomach pain has been reported in several cases of confirmed Haff disease following ingestion of boiled crayfish (Diaz, 2015).
    b) In a series of confirmed Haff disease cases reported in China from 1997 to 2014, stomach pain occurred in 34 of 54 patients following consumption of freshwater pomfret (Colossoma brachypomum) (Diaz, 2015).
    C) DIARRHEA
    1) WITH POISONING/EXPOSURE
    a) In a series of confirmed Haff disease cases reported in China from 1997 to 2014, diarrhea occurred in 18 of 54 patients following consumption of freshwater pomfret (Colossoma brachypomum) (Diaz, 2015).
    D) APTYALISM
    1) WITH POISONING/EXPOSURE
    a) In a series of confirmed Haff disease cases reported in China from 1997 to 2014, dry mouth occurred in 25 of 54 patients following consumption of freshwater pomfret (Colossoma brachypomum) (Diaz, 2015).

Hepatic

    3.9.2) CLINICAL EFFECTS
    A) LIVER ENZYMES ABNORMAL
    1) WITH POISONING/EXPOSURE
    a) Elevations in serum concentrations of aminotransferases and lactate dehydrogenase may develop following Buffalo fish poisoning (Burns et al, 2000) and following ingestion of crayfish (Zhang et al, 2012).
    b) CASE REPORT: A husband and wife developed hepatic transaminase elevations (husband: a peak AST of 1,330 Units/L and ALT of 329 Units/L; wife: a peak AST of 241 Units/L) after ingestion of Buffalo fish (Burns et al, 2000).

Genitourinary

    3.10.2) CLINICAL EFFECTS
    A) RENAL FAILURE SYNDROME
    1) WITH POISONING/EXPOSURE
    a) Renal acidosis and renal failure have been reported as complications of buffalo fish poisoning (CDC, 1998; Solomon, 1990).
    B) ABNORMAL URINE
    1) WITH POISONING/EXPOSURE
    a) After ingestion of Buffalo fish or crayfish, the urine may turn a brown-black or red color (Diaz, 2015; Solomon, 1990; Berlin, 1948).
    b) INCIDENCE: In a series of 27 Brazilian patients with Haff disease, 9 (33%) developed dark urine (dos Santos et al, 2009).

Hematologic

    3.13.2) CLINICAL EFFECTS
    A) DISSEMINATED INTRAVASCULAR COAGULATION
    1) WITH POISONING/EXPOSURE
    a) Buffalo fish poisoning may result in disseminated intravascular coagulation (DIC) (CDC, 1998).

Dermatologic

    3.14.2) CLINICAL EFFECTS
    A) EXCESSIVE SWEATING
    1) WITH POISONING/EXPOSURE
    a) Diaphoresis has been reported in several cases of confirmed Haff disease following ingestion of boiled crayfish (Diaz, 2015).

Musculoskeletal

    3.15.2) CLINICAL EFFECTS
    A) MUSCLE PAIN
    1) WITH POISONING/EXPOSURE
    a) Myalgia has been reported in several cases of confirmed Haff disease following ingestion of buffalo fish and boiled crayfish (Diaz, 2015).
    b) In a series of confirmed Haff disease cases reported in China from 1997 to 2014, myalgia occurred in 46 of 54 patients following consumption of freshwater pomfret (Colossoma brachypomum) (Diaz, 2015).
    B) RHABDOMYOLYSIS
    1) WITH POISONING/EXPOSURE
    a) Following ingestion of buffalo fish, symptoms of muscle stiffness, tenderness, and rigidity usually occur 6 to 24 hours after eating contaminated food. Creatine kinase is usually markedly elevated, with a CK-MB fraction of less than 5%. Levels of other muscle enzymes (lactate dehydrogenase, glutamate pyruvate transaminase, glutamate oxalate transaminase, and myoglobin) may also be elevated (Buchholz et al, 2000; CDC, 1998; Solomon, 1990; Berlin, 1948). Symptoms of muscle stiffness and rigidity, myalgias, and elevated liver enzyme and creatine kinase concentrations have also been reported following consumption of crayfish and Brazilian river fishes, including Mylossoma species (pacu [silver dollar fish]), Colossoma macropomum (tambaqui [black-finned colossoma]), and Piaractus brachypomus (pirapitinga [freshwater pompano]) (Zhang et al, 2012; dos Santos et al, 2009).
    b) INCIDENCE: In a series of 27 Brazilian patients with Haff disease, all patients developed myalgia and rhabdomyolysis within 24 hours of eating fish; 13 (48%) patients reported muscle stiffness, and 10 (37%) had muscle contracture (dos Santos et al, 2009).
    c) CASE REPORT: Rhabdomyolysis was reported in two sisters eating contaminated buffalo fish. Eight hours after ingestion of the fish, both patients developed severe arm rigidity and had marked elevations in serum creatine kinase of 25,000 IU/L and 9454 IU/L, respectively (CDC, 1998).
    d) CASE REPORT: A 33-year-old man developed symptoms after eating buffalo fish purchased from the same market as the above case. The man was admitted to the hospital complaining of chest pain radiating to the left arm. Monitoring of the patient revealed no cardiac abnormalities but the patient did have an elevated serum creatine kinase of 4140 IU/L with a CK-MB fraction of 1.4% . The wife, who also ingested some fish, was asymptomatic (CDC, 1998).
    e) CASE REPORT: A husband and wife, aged 66 and 58 years, became ill 6 hours after ingestion of ground buffalo fish and carp. The patients developed diffuse body aches and muscle stiffness, with creatine kinase measurements exceeding 17,700 IU/L in both cases, with CK-MB fractions of 4.8% and 4.5%, respectively (CDC, 1998). Another couple also developed rhabdomyolysis after ingestion of Buffalo fish (Burns et al, 2000).
    f) CASE REPORT: Twenty-one hours after eating buffalo fish, an 87-year-old man awoke with extreme stiffness and generalized muscle tenderness. Measured creatine kinase was 2226 IU/L with a CK-MB of 2.1%. The patient was treated symptomatically with fluids and analgesics. The patient suffered residual leg weakness for 6 months following the incident (CDC, 1998).
    g) CASE REPORTS: Two patients (husband and wife, aged 65 and 56 years, respectively), developed mild proximal muscle weakness and tenderness approximately 24 hours after eating baked salmon. Laboratory data, obtained 6 days later, showed elevated creatine kinase concentrations of 411 and 285 units/L, respectively. The muscle weakness gradually resolved within 2 weeks after onset (Langley & Bobbitt, 2007).
    h) CASE SERIES: Several patients developed nausea, vomiting, chest pain, dyspnea, and diaphoresis within 3 to 16 hours after eating crawfish purchased at the same seafood restaurant/market. All of the patients had elevated creatine phosphokinase concentrations of 6000 to 8600. With supportive care, all of the patients recovered without sequelae. A subsequent literature review identified this outbreak as characteristic of Haff disease, typically observed with buffalo fish poisoning (Krishna & Wood, 2001).
    i) CASE SERIES: Haff disease was reported in 5 adults following consumption of crayfish. All 5 patients experienced myalgia, and chest and back pain. Two patients experienced whole-body numbness, 1 patient experienced muscle stiffness, and 1 patient developed dyspnea. Laboratory evaluations revealed elevated liver enzymes and serum creatine kinase concentrations (ranging from approximately 2515 to 8487 units/L) in all patients. With supportive care, all of the patients recovered and were discharged within 6 days post-ingestion (Zhang et al, 2012).
    C) ASTHENIA
    1) WITH POISONING/EXPOSURE
    a) INCIDENCE: In a series of 27 Brazilian patients with Haff disease, 11 (41%) reported weakness and 8 (30%) described malaise (dos Santos et al, 2009).
    3.15.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) RHABDOMYOLYSIS
    a) Mice were fed hexane soluble extracts from the cooked buffalo fish obtained from freshwater sources in Missouri and Louisiana. Although the fish test was negative for any biotoxins, saxitoxin and cyanobacterial toxins, the mice had discolored urine and behavioral changes consistent with muscle damage (Buchholz et al, 2000).

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) Monitor serial serum creatine kinase, electrolytes, and renal function tests. Monitor liver enzymes, CBC, and INR in patients with severe toxicity.
    B) Obtain an ECG in symptomatic patients.
    C) Frequent monitoring of vital signs and support of vital functions (pulse, blood pressure, and respirations) may be required.
    D) Monitor oxygenation in symptomatic patients.
    E) Monitor urinalysis and urine output.
    4.1.2) SERUM/BLOOD
    A) BLOOD/SERUM CHEMISTRY
    1) Monitor serial serum creatine kinase, electrolytes, and renal function tests. Monitor liver enzymes, CBC, and INR in patients with severe toxicity.
    4.1.3) URINE
    A) Monitor urinalysis and urine output.
    4.1.4) OTHER
    A) OTHER
    1) MONITORING
    a) Frequent monitoring of vital signs and support of vital functions (pulse, blood pressure, and respirations) may be required.
    b) Monitor oxygenation in symptomatic patients.
    2) ECG
    a) Obtain an ECG in symptomatic patients.

Treatment

Life Support

    A) Support respiratory and cardiovascular function.

Patient Disposition

    6.3.1) DISPOSITION/ORAL EXPOSURE
    6.3.1.1) ADMISSION CRITERIA/ORAL
    A) Patients with significant rhabdomyolysis, persistent vomiting, or other systemic effects should be admitted.
    6.3.1.2) HOME CRITERIA/ORAL
    A) Patients who are asymptomatic after consumption of buffalo fish may be monitored at home.
    6.3.1.3) CONSULT CRITERIA/ORAL
    A) Consult a medical toxicologist for assistance with medical management in patients who develop significant toxicity or in whom the diagnosis is unclear. Notify your local health department of suspected cases.
    6.3.1.5) OBSERVATION CRITERIA/ORAL
    A) Symptomatic patients should be referred to a healthcare facility for evaluation and treatment. Patients should be observed in a medical facility until CK is declining and signs and symptoms of toxicity are improved.

Monitoring

    A) Monitor serial serum creatine kinase, electrolytes, and renal function tests. Monitor liver enzymes, CBC, and INR in patients with severe toxicity.
    B) Obtain an ECG in symptomatic patients.
    C) Frequent monitoring of vital signs and support of vital functions (pulse, blood pressure, and respirations) may be required.
    D) Monitor oxygenation in symptomatic patients.
    E) Monitor urinalysis and urine output.

Oral Exposure

    6.5.1) PREVENTION OF ABSORPTION/PREHOSPITAL
    A) GENERAL
    1) The role of gastric decontamination in buffalo fish poisoning is unknown. Although vomiting may occur soon after ingestion, many patients may not present until 6 to 24 hours after ingestion, making gastrointestinal decontamination of questionable benefit.
    6.5.2) PREVENTION OF ABSORPTION
    A) SUMMARY
    1) The role of gastric decontamination in buffalo fish poisoning is unknown. Although vomiting may occur soon after ingestion, many patients may not present until 6 to 24 hours after ingestion, making gastrointestinal decontamination of questionable benefit.
    6.5.3) TREATMENT
    A) MONITORING OF PATIENT
    1) Monitor serial serum creatine kinase, electrolytes, and renal function tests. Monitor liver enzymes, CBC, and INR in patients with severe toxicity.
    2) Obtain an ECG in symptomatic patients.
    3) Frequent monitoring of vital signs and support of vital functions (pulse, blood pressure, and respirations) may be required.
    4) Monitor oxygenation in symptomatic patients.
    5) Monitor urinalysis and urine output.
    B) FLUID/ELECTROLYTE BALANCE REGULATION
    1) Initial administration of large volumes of fluid may help to prevent myoglobin toxicity to the renal tubules (CDC, 1998). Replace electrolytes as needed.
    C) RHABDOMYOLYSIS
    1) SUMMARY: Early aggressive fluid replacement is the mainstay of therapy and may help prevent renal insufficiency. Diuretics such as mannitol or furosemide may be added if necessary to maintain urine output but only after volume status has been restored as hypovolemia will increase renal tubular damage. Urinary alkalinization is NOT routinely recommended.
    2) Initial treatment should be directed towards controlling acute metabolic disturbances such as hyperkalemia, hyperthermia, and hypovolemia. Control seizures, agitation, and muscle contractions (Erdman & Dart, 2004).
    3) FLUID REPLACEMENT: Early and aggressive fluid replacement is the mainstay of therapy to prevent renal failure. Vigorous fluid replacement with 0.9% saline (10 to 15 mL/kg/hour) is necessary even if there is no evidence of dehydration. Several liters of fluid may be needed within the first 24 hours (Walter & Catenacci, 2008; Camp, 2009; Huerta-Alardin et al, 2005; Criddle, 2003; Polderman, 2004). Hypovolemia, increased insensible losses, and third spacing of fluid commonly increase fluid requirements. Strive to maintain a urine output of at least 1 to 2 mL/kg/hour (or greater than 150 to 300 mL/hour) (Walter & Catenacci, 2008; Camp, 2009; Erdman & Dart, 2004; Criddle, 2003). To maintain a urine output this high, 500 to 1000 mL of fluid per hour may be required (Criddle, 2003). Monitor fluid input and urine output, plus insensible losses. Monitor for evidence of fluid overload and compartment syndrome; monitor serum electrolytes, CK, and renal function tests.
    4) DIURETICS: Diuretics (eg, mannitol or furosemide) may be needed to ensure adequate urine output and to prevent acute renal failure when used in combination with aggressive fluid therapy. Loop diuretics increase tubular flow and decrease deposition of myoglobin. These agents should be used only after volume status has been restored, as hypovolemia will increase renal tubular damage. If the patient is maintaining adequate urine output, loop diuretics are not necessary (Vanholder et al, 2000).
    5) URINARY ALKALINIZATION: Alkalinization of the urine is not routinely recommended, as it has never been documented to reduce nephrotoxicity, and may cause complications such as hypocalcemia and hypokalemia (Walter & Catenacci, 2008; Huerta-Alardin et al, 2005; Brown et al, 2004; Polderman, 2004). Retrospective studies have failed to demonstrate any clinical benefit from the use of urinary alkalinization (Brown et al, 2004; Polderman, 2004; Homsi et al, 1997).
    D) BRONCHOSPASM
    1) BRONCHOSPASM SUMMARY
    a) Administer beta2 adrenergic agonists. Consider use of inhaled ipratropium and systemic corticosteroids. Monitor peak expiratory flow rate, monitor for hypoxia and respiratory failure, and administer oxygen as necessary.
    2) ALBUTEROL/ADULT DOSE
    a) 2.5 to 5 milligrams diluted with 4 milliliters of 0.9% saline by nebulizer every 20 minutes for three doses. If incomplete response, administer 2.5 to 10 milligrams every 1 to 4 hours as needed OR administer 10 to 15 milligrams every hour by continuous nebulizer as needed. Consider adding ipratropium to the nebulized albuterol; DOSE: 0.5 milligram by nebulizer every 30 minutes for three doses then every 2 to 4 hours as needed, NOT administered as a single agent (National Heart,Lung,and Blood Institute, 2007).
    3) ALBUTEROL/PEDIATRIC DOSE
    a) 0.15 milligram/kilogram (minimum 2.5 milligrams) diluted with 4 milliliters of 0.9% saline by nebulizer every 20 minutes for three doses. If incomplete response administer 0.15 to 0.3 milligram/kilogram (maximum 10 milligrams) every 1 to 4 hours as needed OR administer 0.5 mg/kg/hr by continuous nebulizer as needed. Consider adding ipratropium to the nebulized albuterol; DOSE: 0.25 to 0.5 milligram by nebulizer every 20 minutes for three doses then every 2 to 4 hours as needed, NOT administered as a single agent (National Heart,Lung,and Blood Institute, 2007).
    4) ALBUTEROL/CAUTIONS
    a) The incidence of adverse effects of beta2-agonists may be increased in older patients, particularly those with pre-existing ischemic heart disease (National Asthma Education and Prevention Program, 2007). Monitor for tachycardia, tremors.
    5) CORTICOSTEROIDS
    a) Consider systemic corticosteroids in patients with significant bronchospasm. PREDNISONE: ADULT: 40 to 80 milligrams/day in 1 or 2 divided doses. CHILD: 1 to 2 milligrams/kilogram/day (maximum 60 mg) in 1 or 2 divided doses (National Heart,Lung,and Blood Institute, 2007).
    E) INFECTIOUS DISEASE NOTIFICATION
    1) REPORTING: All cases of buffalo fish poisoning should be reported to the state health departments, who in turn are requested to report to the Foodborne and Diarrheal Diseases Branch, Division of Bacterial and Mycotic Diseases, National Center for Infectious Diseases, CDC. Telephone: 404-639-2206.

Enhanced Elimination

    A) HEMODIALYSIS
    1) No studies have addressed the utilization of extracorporeal elimination techniques in poisoning with this agent. However, hemodialysis may be considered in cases of severe renal failure due to buffalo fish toxins.

Range Of Toxicity

Summary

    A) TOXICITY: Severity of illness may be related to the amount of toxin ingested. It is not known whether toxicity is dependent on the size of the fish.

Minimum Lethal Exposure

    A) GENERAL/SUMMARY
    1) The case fatality rate of "Haff Disease" was reported to be approximately 0.5% to 1% in an outbreak in East Prussia, with 13 fatalities (Jeddeloh, 1939).

Pharmacology Toxicology

Toxicologic Mechanism

    A) The chemical and pharmacologic properties of the buffalo fish toxin are unknown. It has been postulated that the toxin may originate in fat-soluble toxins present in blue green algae that the fish eat, but this has not yet been confirmed (Leshtchenko et al, 1965).

References

General Bibliography

    1) Anon: Freshwater buffalo fish products from Stroller fisheries. Stoller Fisheries. Spirit Lake, IA, USA. 2001. Available from URL: http://www.sfishinc.com/fisht4.htm.
    2) Berlin R: Haff disease in Sweden. Acta Medica Scandinavica 1948; 129:560-572.
    3) Brown CV, Rhee P, Chan L, et al: Preventing renal failure in patients with rhabdomyolysis: do bicarbonate and mannitol make a difference?. J Trauma 2004; 56(6):1191-1196.
    4) Buchholz U, Mousin E, & Dickey R: Haff Disease: From the Baltic sea to the US Shore. Emerg Infect Diseases 2000; 6(2):192-195.
    5) Burns D, Snyder L, Kirk M, et al: Rhabdomyolysis from Buffalo fish consumption (abstract). J Toxicol Clin Toxicol 2000; 38(5):513.
    6) CDC: Haff disease associated with eating buffalo fish, United States, 1997. CDC: MMWR 1998; 47:1091-1093.
    7) Camp NE: Drug- and toxin-induced Rhabdomyolysis. J Emerg Nurs 2009; 35(5):481-482.
    8) Criddle LM: Rhabdomyolysis. Pathophysiology, recognition, and management. Crit Care Nurse 2003; 23(6):14-22, 24-26, 28.
    9) Diaz JH: Global incidence of rhabdomyolysis after cooked seafood consumption (Haff disease). Clin Toxicol (Phila) 2015; 53(5):421-426.
    10) Erdman AR & Dart RC: Rhabdomyolysis. In: Dart RC, Caravati EM, McGuigan MA, et al, eds. Medical Toxicology, 3rd ed. Lippincott Williams & Wilkins, Philadelphia, PA, 2004, pp 123-127.
    11) Herman TE & McAlister WH: Epiglottic enlargement: Two unusual cases.. Pediatr Radiol. 1991; 21:139-40.
    12) Homsi E, Barreiro MF, Orlando JM, et al: Prophylaxis of acute renal failure in patients with rhabdomyolysis. Ren Fail 1997; 19(2):283-288.
    13) Huerta-Alardin AL, Varon J, & Marik PE: Bench-to-bedside review: Rhabdomyolysis -- an overview for clinicians. Crit Care 2005; 9(2):158-169.
    14) Jeddeloh BZ: Haffkrankheit. In: Czerny A, Mueller F, von Pfaundler M et al (eds). Ergebnisse der inneren Medizin und Kinderheilkunde, Springer-Verlag, Berlin, Germany, 1939, pp 138-182.
    15) Krishna N & Wood J: It looked like a myocardial infarction after eating crawfish... Ever heard of Haff Disease?. Louisiana Morbidity Report 2001; 12(3):1-2.
    16) Langley RL & Bobbitt WH: Haff disease after eating salmon. South Med J 2007; 100(11):1147-1150.
    17) Leshtchenko PD, Khoroshilova NV, & Slipchenko LM: Observation of Haffs-uchs disease cases. Vopr Pitan 1965; 24:73-76.
    18) National Asthma Education and Prevention Program: Expert Panel Report 3 (EPR-3): Guidelines for the Diagnosis and Management of Asthma-Summary Report 2007. J Allergy Clin Immunol 2007; 120(5 Suppl):S94-S138.
    19) National Heart,Lung,and Blood Institute: Expert panel report 3: guidelines for the diagnosis and management of asthma. National Heart,Lung,and Blood Institute. Bethesda, MD. 2007. Available from URL: http://www.nhlbi.nih.gov/guidelines/asthma/asthgdln.pdf.
    20) Polderman KH: Acute renal failure and rhabdomyolysis. Int J Artif Organs 2004; 27(12):1030-1033.
    21) Solomon M: Haff disease [letter]. Arch Int Med 1990; 150:683.
    22) Vanholder R, Sever MS, Erek E, et al: Rhabdomyolysis. J Am Soc Nephrol 2000; 11(8):1553-1561.
    23) Walter LA & Catenacci MH: Rhabdomyolysis. Hosp Physician 2008; 44(1):25-31.
    24) Zhang B , Yang G , Yu X , et al: Haff disease after eating crayfish in east China. Intern Med 2012; 51(5):487-489.
    25) dos Santos MC, de Albuquerque BC, Pinto RC, et al: Outbreak of Haff disease in the Brazilian Amazon. Rev Panam Salud Publica 2009; 26(5):469-470.