VIII.

PENATALAKSANAAN KERACUNAN MAKANANDAN MINUMAN

Tempe Bongkrek
Tempe bongkrek adalah sejenis makanan yang dibuat dan ampas kelapa parut yang
telah diperas santannya untuk pembuatan minyak kelapa. Cara pembuatannya melalui
proses fermentasi dengan menggunakan ragi Rhizopus Oligosporus. Tempe bongkrek
merupakan makanan khas masyarakat di Jawa Tengah khususnya di daerah Banyumas dan
sekitarnya.
Proses terjadinya racun dalam tempe bongkrek:
Pada proses fermentasi adonan tempe bongkrek akan menimbulkan panas, sehingga
suhu adonan akan naik sampai 400 C. dalam keadaan suhu tersebut mengakibatkan
timbulnya bakteri, terutama Pseudomonas Cocovenans yang menghasilkan enzim, yang
dapat menghidrolisis minyak menjadi gliserol dan asam lemak (terutam asam oleat). Dan
asam oleat ini membentuk asam bongkrek dan toksoflavin.
Mekanisme Toksisitas:
Asam bongkrek dan toksoflavin menyebabkan inbisi terhadap enzirn-enzim
mitokondria, mengganggu mekanisme fosforilasi oksidatif, menghambat sintesis ATP,
sehingga dapat mengganggu metabolisme glikogen sehingga menyebabkan hipoglikemia.
Sifat racun asam bongkrek dan toksoflavin, tahan terhadap panas (termostabil)
sampai suhu titik leleh 117° C. Oleh karena itu racun tempe bongkrek tetap aktif dan
berbahaya walaupun dimasak/digoreng.
Gejala-gejala keracunan tempe bongkrek:
1. Mula-mua korban mersa badannya kurang segar, perut kejang, muntah dan
mencret.
2. Pusing kepala, banyak mengeluarkan keningat, kejang-kejang.
3. Kesadarannya menurun, bila tidak segena ditolong, korban akan mati dalam
waktu beberapa jam.
Pengobatan:
1. Terapi suportif
2. Dekontaminasi : pengosongan lambung, arang aktif, Iaksatif (bila tidak diare)
3. infus glukosa, injeksi vitamin B komplek, thisulfat.

Pencegahan:
1. Menjaga kebersihan dalam pembuatannya dengan menghindari kontaminasi oleh
bakteri atau bahan lain yang bersifat racun.
2. Menggunakan ampas kelapa parut yang masih baru.

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 3. Sebelum dikonsumsi, sebaiknya dijemur dulu dibawah sinar matahari beberapa
jam untuk menghilangkan racun toksoflavin, sedang asam bongkreknya tidak bisa
hilang dengan dijemur panas matahari.

BOTULISM
Olga F. Woo, PharmD

Botulism dates back to the 1700s as a recognized cause of fatal food poisoning. Rare
outbreaks still occur in the USA, usually associated with improper home canning of foods.
Recently, new sources of botulism have been discovered, such as improperty prepared or
stored pot pies, fried onions, and baked potatoes; wound botulism in parenteral drug abusers
and infant botulism.
I. MechanIsm of toxicity
A. Botulism is caused by a heat-lablle neurotoxin (botulin) produced by the bacteria
Clostridium botulinum. Different strains of the bacterium produce 6 dIstinct exotoxins:
A. B.C, D, E. and F; types A, B. E, and F are most frequently involved in human
disease. Botuiln toxin irreversibly binds to cholinergic nerve terminals and prevents
acetylcholine release from the axon. Severe muscle weakness results, and death is
due to respiratory faillure.
B. Botuilnum spores are ubiquitous in nature but are not dangerous unless they are
allowed to germinate in an anaerobic environment with a pH greater than 4.6.
Incompletely cooked foods left out at ambient temperatures for more than 16 hours
may produce lethal amounts of botulin toxin. The spores can be destroyed by
pressure cooking at a temperature of at least 120 C (250 F) for 30 minutes. The toxin
can be destroyed by balling at 10o C (212 F) for one minute or heating at 60 C (176 •F)
for 20 mlnutes.
II. Toclc dose. Botuftn toxin is extremely potent; as little as one taste of botulln-contaminated
food (approximately 0.05 mcg of toxin) may be fatal.
III. Clinical presentation
A. Classic botulism occurs after Ingestion of preformed toxin in contaminated food. The
incubation period is usually 181036 hours after Ingestion but can vary from a few
hours 108 days. The earlier the onset of symtoms, the more severe the illness. Initial
symptoms may suggest a flulike syndrome: sore throat, dry mouth, and
gastrointestinal upset. Later, diplopia, ptosis, dysarthria, and other cranial nerve
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 weaknesses occur, followed by progressive descending paralysis and finally
respiratory arrest. The patient’s mentation is clear, and there is no sensory loss. Pupils
may be dilated and unceactive or normal. Constipation may occur.
B. Infant botulism is not caused by ingestion of preformed toxin but by in vivo production
of toxin in the immature infant gut. Infants who are breast-ted and those given honey
may have a higher risk of developing the disease, which is characterized by
hypotonia, constipation, tachycardia, difficulty in feeding, head lag, and diminished
gag reflex. Ills rarely fatal, and infants usually recover strength within 4-6 weeks.
C. Wound botulism occurs mostly in young adult Intravenous drug abusers.Theorganism
germinates in an Infected injection site and produces toxin In vivo. Typical
manifestations of botulism occur after an incubation period of 4-14 days.
IV. Diagnosis. Diagnosis is based on a high Index of suspicion in any patient with a dry sore
throat, clinical findings of descending cranial nerve palsies or gastroenteritis, and a history
of Ingestion of home-canned food. Symptoms may be slow In onset but are sometimes
rapidly progressive. Electro-myography may reveal normal conduction velocity but
decreased motor action potential and no incremental response to repetitive stimulation.
A. Specific levels. Diagnosis is confirmed by determination of the toxin In serum or stool;
although these tests are usef ul for public health investigation. they cannot be used to
determine initial treatment because analysis takes more than 24 hours to perform.
Obtain serum, stool, vomitus, gastric contents, and suspect food for toxin analysis by
the local or state health department. The results may be negative if the samples were
collected late or the quantity of toxin is small.
B. Other useful laboratory studies. CBC, electrolytes, blood sugar, arterial blood gases.
electromyogram, CSF if CNS infection is suspected.
V. Treatment
A. Emergency and supportive measures
1. Obtain arterial blood gases and observe closely for respiratory weakness;
respiratory arrest can occur abruptly.
2. Maintain the airway and assist ventilation If necessary (seep 2).
B. Specific drugs and antidotes
1. Classic and wound botulism
a. Botulin antitoxin (see p 297) binds the circulating free toxin and prevents the
progression of Illness; however, it does not reverse established neurologic
manifestations. Available antitoxins are bivalent (AB) and trivalent (ABE);
trivalent antitoxin is preferred unless the exact toxin is known.

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 (1) Consult the local health department or Centers for Disease Control,
Atlanta, Ga; telephone (404) 329-2888 (24-hour number).
(2) Determine sensitivity 10 horse serum prior to treatment.
(3) Administer 1 vial every 4 hours for at least 4-5 doses or until no toxin is
present in serum.
b. Guanidine may be useful as adjunctive therapy in enhancing release of
acetylcholine at the nerve terminal and improving ocular and limb paralysis but
not respiratory paralysis.The dose is 15-50 mg/kg/d divided into 4-5 doses..
2. Infant botulism. Antitoxin is not recommended for infant botulism. The use of oral
antibiotics and cathartics is controversiaL
C. Decontamination
1. Induce emesis or perform gastric lavage (see p 42) if recent known Ingestion has
occurred.
2. Administer activated charcoal and acathartic (see p45).
D. Enhanced elimination. There is no role for enhanced elimination; the toxin binds
rapidly to nerve endings, and any free toxin can be readily detoxified with antitoxin.

CYANIDE
Paul D. Blanc, MD

Cyanide is a highly reactive chemical with a variety of uses, Including chemical synthesis,
laboratory analysis, and metal plating. Aliphatic nitriles (acryllonitrile, propionitrile; used in
plastics manufacturing are metabolized to cyanide. The vasodilatoc drug nitroprusside
releases cyanide on exposure to light. Natural Sources of cyanide (amygdaiin and many
other cyanogenic glycosfces) are found in apricot pits, cassava, and many other plants and
seeds.
Hydrogen cyanide is a gas easily generated by mixing acid with Cyanide salts and is a
Common combustion by-procju of burning plastics, wool, and many other natural and
Synthetic products. Hydrogen cyanide Poisoning is an important cause of death in fires, and
deliberate cyanide exposure remains an important instrument of homicide and suicide.
I. Mechanism of toxicity. Cyanide is a chemical asphyxiant; by irreversibly binding to
cellular cytochrome oxidase, It blocks the aerobic utilization of oxygen. Unbound
cyanide Is detoxified by metabolism to thiocyanate, a much less toxic Compound that
is slowly excreted in the urine.

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II. Toxic dose
A. Exposure to hydrogen cyanide gas (HCN) at low levels (150-200 ppm) can be
rapidly fatal. The OSHA permissible exposure limit (PEL) for HCN is 10 ppm (11
mg/m3) as an 8-hour time-weighted average.
B. Adult ingestion of as little as 200 mg of the sodium or Potassium salt may be fatal.
C. Acute cyanide poisoning is relatively rare with nitroprusside (infusion at normal
infusion rates) or after Ingestion of seeds (unless they have been pulverized).
III. Clinical presentation. Abrupt onset of profound toxic effects shortly after exposure is
the hailmaric of cyanide Poisoning. Symptoms include headache, nausea, dyspnea,
and confusion. Syncope, seizures, coma, agonal respirations, and cardiovascular
collapse ensue rapidly.
A. Brief delay may occur if the cyanide is ingested as a salt, especially it it is in a
capsule or if there is food in the stomach.
B. Delayed symptoms may also occur after acrylonitrile exposure because of
metabolism to Cyanide.
C. Chronic neurologic sequelae may follow severe cyanide Poisoning.
IV. Diagnosis. Diagnosis is based on a history of exposure or the presence of rapidly
progressive symptoms and signs. Lactic acidosis is often present. The measured
venous oxygen saturation may be elevated owing to blocked Cellular oxygen
Consumption. The classic bitteratmond aroma of hydrogen cyanide may or may not
be noted, because of genetic variability in the ability to appreciate the smell.
A. Specific levels. Cyanide determinations are rarely of use in emergency
management, because they cannot be performed rapidly enough to alter Initial
treatment. They must be interpreted with caution because of a variety of
complicating technical factors.
1. Levels higher than 0.5-1 mg/L are considered toxic.
2. Smokers may have Ievel up to 0.1 mg/t..
3. Rapid nitroprusside infusion may produce levels as high as 1 mg/L.
B. Other useful laboratory studies. CBC, electrolytes, glucose, arterial blood gas,
carboxyhemoglobin (if smoke inhalation exposure), EGG.
V. Treatment
A. Emergency and supportive measures. Treat all cyanide exposures as potentially
lethal.
1. Maintain the airway and assist ventilation if necessary (see P 2). Administer
supplemental Oxygen
2. Treat coma (p 17), hypotension(p 14), and seizures(p21) if they occur.
3. Start an intravenous line and monitor the patien’s vital signs and EGG Closely.

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B. Specific drugs and antidotes
1. The Lilly cyanide antidote kit consists of amyl and sodium nitrites (see p328),
which produce cyanide-scavenging methemoglobinemia, and sodium
thlosulfate (see p 340), which accelerates the conversion of cyanide to
thiocyanate.
a. Break a pearl of amyl nitrite under the nose of the victim; and administer
sodium nitrite, 300 mg IV (6 mg/kg for children). Caution: Nitrite-induced
methemoglobinemia can be extremely dangerous and even lethal. Nitrite
should not be given if the symptoms are mild or if the diagnosis is
uncertain.
b. Administer sodium thiosuifate, 12.59 IV. Thiosulfate is relatively benign
and may be given empirically if the diagnosis is uncertain.
2. The most promising alternative antidote Is hydroxocobalamin (see p 316). It is
currently undergoing investigational trials in the USA.
3. Hyperbaric oxygen has no established role in cyanide poisoning treatment.
C. Decontamination
1. lnhalation. Remove victim from hydrogen cyanide exposure and give
supplemental oxygen, if available. Rescuers should wear protective self-
contained breathing apparatus.
2. Skin. Remove all contaminated clothing and wash affected areas with copious
soap and water.
3. Ingestion
a. Immediately place a gastric tube arid administer activated charcoal, then
perform gastric lavage (seep 43). Do not induce emesis unless victim is
more than 20 minutes from a medical facility.
b. Administer additional activated charcoal arid a cathartic (see p 45) after
the lavage. Even though charcoal has a relatively low affinity for cyanide. It
is effective for the doses of cyanide (100-300 mg) of ten Ingesled.
D. Enhanced elimination. There is no role for hemodialysis or hemoperfusian in
cyanide poisoning treatment. Hemodialysis may be indicated in patients with renal
Insufficiency who develop high thlocyanate levels while on extended nitroprusside
therapy.

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FOOD POISONING:
BACTERIAL.
James F. Buchanan, PharmD

Foodborrie illness is one of the most common causes of epidemic gastroenteritis. In general,
common bacterial food poisoning is relatively mild and self-limited, with recovery within 24
hours. However, severe and even fatal poisoning may occur with botulism (see p 95).
Poisoning following consumption of fish and shelifish is discussed on p 158.
I. Mechanism of toxicity. Gastroenteritis maybe caused by invasive bacterial infection of
the intestinal mucosa or by a toxin elaborated by bacteria. Bacteria toxins may be
preformed in food that is improperly prepared and improperty stored before use or may
be produced in the gut by the bacteria after they are ingested (Table 11-23).
II. Toxic dose. The toxic dose depends on the type of bacteria or toxin and its
concentration in the ingested food, as well as individual susceptibility or resistance.
Some of the preformed toxins (eg, staphylococcal toxin) are heat resistant and once in
the food are not removed by cookingg or boiling.
III. Clinical presentation. Commonly, a delay or “incubation period” of from 2 hours to 3
days precedes the onset of symptoms (Table II-23).
A. Gastroenteritis is the most common finding, with nausea, vomiting, abdominal
cramps, and diarrhea. Significant fluid and electrolyte abnormalities may occur,
especially in young children or elderly patients.
B. Fever, bloody stools, and focal leukocytosis are common with invasive bacterial
infections.
IV. Diagnosis. Bacterial food poisoning is often difficult to distinguish from common viral
gastroenteritis, unless the incubation period is short and there are multiple victims who
are similar foods at one large gathering. The presence of many white blood cells in a
stool smear suggests invasive bacterial infection. With any epidemic gastroenteritis,
consider other foodborne Illnesses, such as seafood (see below), botulism (p 95), and
mushrooms (p 210).
A. Specific levels. There are no specific assays that will assist clinical management.
1. Stool culture may differentiate Salmonella, Shigella, and Campylobac ter
lnfections.
2. Food samples should be saved for bacterial culture and toxin analysis, primarily
for use by public health investigators.

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 B. Other useful laboratory Studies CBC, electrolytes, glucose, BUN, creatinine, liver
function tests.
V. Treatment
A. Emergency and supportive measures
1. Replace fluid and electrolyte losses with intravenous saline or other crystalloid
solutions (patients with, mild illness may tolerate oral rehydration). Patients with
hypotension may require large-volume intravenous fluid resuscitation (seep 14).
2. Antiemetic agents are acceptable for symptomatic treatment, but antidiarrheal
agents such as Lomotil (diptienoxylate plus atropine; see p 190) should not be
used because they may prolong the course of the infection.
B. Specific drugs and antidotes. There are no specific antidotes. In patients with
invasive bacterial infection, antibiotics may be used once the stool culture reveals
the specific bacteria responsible.

C. Decontamination. There is no role for gut decontamination

D. Enhanced elimination. There is no role for enhanced removal procedures

POISONING:
FISH AND SHELLFISH
James F. Buchanan, PharmD

A variety of toxins may produce illness alter ingestion of fish or shellfish. The most common
types of seafood-related toxins include ciguatera, scombroid, neurotoxic shellfish poisoning,

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paralytic shellfish poisoning, and tetrodotoxin. ShelIfish-induced bacterial diarrhea is
described below.
I. Mechanism of toxicity. The mechanism varies with each toxin. The toxins are all
heat-stable; therefore, cooking the seafood does not prevent illness.
A. Ciguatera. The toxin is produced by dinoflagellates that are then consumed by
reef fish. The mechanism of intoxication is unknown.
B. Scombroid. Scrombotoxin is a mixture of histamine and other histamine-like
compounds produced when histidine in fish tissue decomposes.
C. Neurotoxic shellfish. The mechanism is unknown. Neurotoxins are thought to
stimulate postganglionic cholinergic neurons.
D. Paralytic shellfish. Dinoflageliates (“red tide”) produce saxitoxin, which is
concentrated by filter-feeding clams and mussels. Saxitoxin blocks sodium
conductance and neuronal transmission in skeletal muscles.
E. Tetrodotoxin. Tetrodotoxin, produced in the skin of puffer fish, California newts,
and some South American frogs. is similar to saxitoxin and blocks sodium
conductance and neuronai transmission In skeletal muscles.
II. Toxic dose. The concentration of toxin varies widely depending on geographic and
seasonal factors. The amount of toxin necessary to produce symptoms is
unknown. Saxitoxin is extremely potent; the estimated lethal dose in humans is
0.3-1 mg, and contaminated mussels may contain 15-20 mg.
III. Clinical presentation. The onset of symptoms and clinical manifestations vary with
each toxin (Table 11-24). In the majority of cases the seafood appears normal with
no adverse smell or taste (scombroid may have a peppery taste).
A. Ciguatera. Intoxication produces vomiting and watery diarrhea 1-6 hours after
ingestion, followed by headache, malaise, myalgias, paresthesias of the mouth
and extremities, ataxia, blurred vision, photophobia, reversal of hot and cold
sensation, hypOtelision, bradycardia, and rarely, seizures and respiratory
arrest.
B. Scombrold. Symptoms begin rapidly (minutes to 3 hours) after ingestion.
Gastroenteritis, headache, and skin flushing are sometimes accompanied by
urticaria and bronchospasm.
C. Neurotoxic shellfish. Onset is within a few minutes to 3 hours. Gastroenteritis is
accompanied by parosthesias of the mouth, face, and extremities; muscular
weakness; and respiratory arrest.
D. Paralytic shellfish. Vomiting, diarrhea, and facial paresthesias usually begin
within 30 minutes of ingestion. Headache, myalgias, dysphagia,

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 weakness, and ataxia have been reported. In serious cases respiratory arrest
may occur after 1-1 hours.
E. Tetrodotoxin. Symptoms occur within 30-40 minutes after Ingestion, with
vomiting and paresthesias. Salivation, twitching, diaphoresis, weakness, and
dysphagia are reported. Hypotension, bradycardia, and respiratory arrest may
occur up to 6-24 hours after Ingestion.
IV.Diagnosis. The diagnosis depends on a history of ingestion and is more likely to be
recognized when multiple victims present after consumption of a common meal.
Scombroid may be confused with an allergic reaction because of the histamine-
induced urticaria.
A. Specific levels are not generally available. However, when epidemic poisoning
is suspected, state public health departments or the Centers for Disease
Control can analyze suspect for toxins.
B. Suggested laboratory tests: CBC, electrolytes, glucose, BUN, creatinine,
arterial blood gases, electrocardiographic monitoring.
V. Treatment
A. Emergency and supportive measures. Most cases of mild poisoning are self-
limited and require no specific treatment. However, because of the risk of
respiratory arrest, all patients should be observed for several hours.
1. Maintain the airway and assist ventilation if necessary (see p 2).
2. Replace fluid and electrolyte losses from gastroenteritis with intravenous
crystalloid fluids (seep 14).
B. Specific drugs and antidotes
1. Antihistamines (eg, diphenhydramine; see p 73) provide effective
symptomatic relief for scombroid intoxication. Rarely, bronchodilators may
also be required.

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 2. There are anecdotal reports of successful treatment of ciguatera with
intravenous mannitol and of scombroid with cimetidine.
C. Decontamination
1. Induce emesis or perform gastric lavage (see p 42) if Ingestion occurred
within the preceding hour. Lavage is preferred if there is evidence of
respiratory weakness or dysphagia.
2. Administer activated charcoal and a cathartic (seep 45).
D. Enhanced elimination. There is no role for enhanced elimination procedures.

ETHANOL
Chris Dutra, MD

Ethanol is found In a variety of commercial liquors, colognes, perfumes, aftershaves,

mouthwashes, some rubbing alcohols, many food flavorings (eg, vanilla, almond, and lemon
extracts), pharmaceutical preparations (eg, elixirs), and many other products. Ethanol is
frequently Ingested recreationally and Is also a common coingestant with other drugs in
suicide attempts.
I. Mechanism of toxicity
A. Central nervous system depression is the principal effect of acute ethanol
Intoxication. Ethanol has additive effects with othercentral nervous system
depressants such as barbiturates, benzodiazeplnes, antldepressants, and
antipsychotics.
B. Hypoglycemia may be due to Impaired gluconeogenesis in patients with depleted
glycogen stores (particularly small children and poorly nourished persons).
C. Ethanol intoxication also predisposes patients to trauma, exposure-Induced
hypothermia, and a number of metabolic derangements that may easily be
overlooked in the “drunk” patient.
II. Toxic dose. The volume of distribution of ethanol is 0.7 L/kg, or about 50 liters in the
average adult. Generally, 0.7 g/kg pure ethanol (approximately 3-4 drinks) will
produce a blood ethanol concentration of 100 mg/dL (0.1 g/dL), considered legally
drunk in most communities.
A. A level of 100 mg/dL is enough to inhibit gluconeogensis and cause hypoglycemia
but by itself is not enough to cause coma.

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 B. The level sufficient to cause deep coma or respiratory depression is highly
variable, depending on the Individual’s degree of tolerance to ethanol: Although
levels above 300 mg/dL usually cause coma in novice drinkers, chronic alcoholics
may be awake with levels in the 500-600 mg/dL range.
III. Clinical presentation
A. Acute intoxication
1. With mild to moderate intoxication, patients exhibit euphoria, mild
incoordination, ataxia, nystagmus, and impaired judgment and reflexes.
Socialinhibitions are decreased, and boisterous or aggressive behavior is
common. Hypoglycemia mayoccur.
2. With deep intoxication, coma, respiratory depression, and pulmonary
aspiration may occur. In these patients, the pupils are usually small and the
temperature, blood pressure, and pulse rate are often decreased.
Rhabdomyolysis may result from prolonged immobilization.
B. Chronic ethanol abuse produces gastrointestinal bleeding from gastrius, ulcers,
Mallory-Weiss tears, or espohageal varices: pancreatitis; hepatitis, cirrhosis and
hepatic encephalopathy hypokalemia, hypophosphatemia, and hypomagnesemia;
thiamine deficiency (Wernicke’s encephalopathy); alcoholic ketoacidosis; and
decreased resistance to infections.
C. Alcohol withdrawal from chronic high level- use usually causes tremulousness,
anxiety, sympathetic nervous system overactIvIty, and convuisions. Occasionally,
this may progress to delirium tremens, a life, threatening syndrome of severe
autonomichyperactivity, hyperthermia, and delirium, which has significant
morbidity and mortality if untreated.
D. Other problems, Ethanol abusers sometimes intentionally or accidentally ingest
ethanol substitutes such as lsopropyl alcohol (see p 181), methanol (p 202), or
ethylene glycol (p 151). In addition, ethanol may serve as the vehicle for
swallowing large numbers of pills in a suicide attempt. Disulfiram (Antabuse. p
143) may cause acute reactIons.
IV. Diagnosis.The diagnosis of ethanol intoxication is usually simple, based on the history
of ingestion, the characteristic smell of fresh alcohol or the fetid odor of metabolic
products, and the presence of nystagmus, ataxla, and altered mental status, it is
imperative to consider other etiologies that may accompany or mimic intoxication,
such as hypoglycemia, head trauma, hypothermia, meningitis, or intoxication with
other drugs or poisons.
A. Specific levels. Ethanol levels are easily and rapidly determined by most hospital
laboratories and, depending on the method used, are accurate and specific.

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 1. In general, there is poorcorrelation between blood levels and clinical
presentation; however, an ethanol level below 300 mg/dL in a comatose
patient should Initiate a search for alternative causes.
2. If ethanol levels are not readily available, the ethanol concentration may be
estimated by calculating the osmolar gap (see p 29).
B. Suggested laboratory studies. COG, glucose, electrolytes, BUN, creatinine,
hepatic transaminases, prothrombin time (PT), magnesium, arterial blood gases,
chest x-ray.
V. Treatment
A. Emergency and supportive measures
1. Acute Intoxication. Treatment is mainly supportive.
a. Protect the airway to prevent aspiration (see p 1), and intubate and assist
ventilation if needed (p4).
b. Give glucose and thiamine (p 340), and treat coma (p 17) and seIzures (p
21) 11 they occur.
c. Correct hypothermia with gradual rewarming (p 18).
d. Most patients will recover within 4-6 hours.
2. Alcohol withdrawal. Treat with benzodlazepines (dlazepam, 2-5 mg IV,
repeated as needed; sea p302) or phenobarbital (130 mg IV slowly. repeated
as needed; seep 334).
B. Specific drugs and antidotes. There is no commercially available specific ethanol
receptor antagonist, but there are anecdotal reports of arousal after administration
of naloxone, 2-5 mg IV (see p 325).
C. Decontamination. Because ethanol is rapidly absorbed, emesis or gastric lavage
is usually not Indicated unless a substantial Ingestion has occurred within 30
minutes of presentation or other drug Ingestion is suspected.
1. Induce emesis or perform gastric lavage (see p 42) if the ingestion was recent
(within 30-45 minutes).
2. Activated charcoal (seep 45) does not efficiently adsorb ethanol but may be
given, especially if other toxins were ingested.
D. Enhanced elimination. Elimination normally occurs at a fixed rate, between 20-40
mg/dL/h. Hemodialysis efficiently removes ethanol, but enhanced removal is
rarely needed because supportive care is usually sufficient. Hemoperfusion and
forced dluresis are not effective.

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METHANOL
IIene B. Anderson, PharmD

Methanol (wood alcohol) is a common ingredient in many solvents, windshield- washing

solutions, duplicating fluids, and paint removers. It is sometimes used as an ethanol
substitute by alcoholics. Although methanol itself produces mainly inebriation, its metabolic
products may cause metabolic acldosis, blindness, and death after a characteristic latent
period of 6-30 hours.
I. Mechanism of toxicity. Methanol is slowly metabolized by alcohol dehydrogenase to
formaldehyde and subsequently by aldehyde dehydrogenase to formic acid (formate).
Systemic acidosis is caused by the formic acid as well as by lactic acid, while
blindness is due primarily to formate. Both ethanol and methanol compete for the
enzyme alcohol dehydrogenase; the preference of this enzyme for metabolizing
ethanol forms the basis for ethanol therapy in methanol poisonings.
II. Toxic dose. The fatal oral dose of methanol is estimated to be 30-240 mL (20-150 g).
The minimum toxic dose is approximately 100 mg/kg. The OSHA workplace
permissible exposure limit (PEL) for inhalation is 200 ppm as an 8-hour time-weighted
average, and the level considered immediately dangerous to life or health (IDLH) is
25,000 ppm.
III. Clinical presentation
A. In the first few hours after ingestion, methanol-intoxicated patients present with
inebriation and gastritis. Acidosis is not usually present because metabolism to
toxic products has not yet occurred. There may be a noticeable elevation in the
osmolar gap (see p 29); an osmolar gap or as little as 10 mosm/L is consistent
with toxic concentrations of methanol.
B. After a latency period of up to 30 hours, severe anion gap metabolic acidosis,
visual disturbances, blindness, seizures, coma, and death may occur. Patients
describe the visual disturbance as haziness or “like standing in a snowfield.” The
latent period is longer when ethanol has been ingested concurrently with
methanol.
IV. Diagnosis. Diagnosis is usually based on the history, symptoms, and laboratory
findings because stat methanol levels are rarely available, Calculation of the osmolar
(see p 29) and anion gaps (see p 30) can be used to estImate the methanol level and
to predict the severity of the ingestion.

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 A. Specific levels
1. Serum methanol levels higher than 20 mg/dL should be considered toxic, and
levels higher than 40 mg/dL should be considered very serious. Following the
latency period, a methanol level of zero does not rule out a serious
Intoxication in a symptomatic patient because all the methanol may already
have been metabolized to formate.
2. Elevated serum formate concentrations may confirm the diagnosis and are a
better measure of toxicity, but formate levels are not yet widely available.
B. Other useful laboratory studies. CBC, electrolytes, glucose, BUN, creatmine,
serum osmolality and osmolar gap, arterial blood gases, ethanol level.
V. Treatment
A. Emergency and supportive measures
1. Maintain the airway and assist ventilation if necessary (see p2).
2. Treat coma (p 17) and seizures (p 21) lf they occur.
3. Treat metabolic acidosis with intravenous sodium bicarbonate (p 296).
Correction of acidosis should be guided by arterial blood gases.
B. Specific drugs and antidotes
1. Ethanol. Start an oral or intravenous infusion of ethanol (see p312) to saturate
the enzyme alcohol dehydrogenase and prevent the formation of methanol’s
toxic metabolites. Ethanol therapy is indicated in patients with the following:
a. A history of a significant methanol ingestion, when methanol serum levels
are not immediately available and the osmolar gap is greater than 5
mosm/L
b. Metabolic acidosis and an osmolar gap greater than 5-10 mosm/L not
accounted for by ethanol.
c. Methanol blood concentration greater than 20 mg/dL
2. Folic acid (see p 314) may enhance the conversion of formate to carbon
dioxide and water. A reasonable dose is 50 mg IV every 4 hours.
3. An experimental drug, 4.methylpyrazole, inhibits alcohol dehydrogenase and
prevents methanol metabolism but is not yet available in the USA.
C. Decontamination
1. Induce emesis or perform gastric lavage (see p 42). Because methanol is
rapidly absorbed, gastric lavage is preferred over emesis if the patient is in the
hospital. Ipecac is used mainly for Initial home or prehospital treatment.
2. Activated charcoal has not been shown to efficiently adsorb methanol. In
addition, charcoal may delay the absorption of orally administered ethanol.

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D. Enhanced elimination. Hemodialysis rapidly removes both methznol and formate.
The indications for dialysis are suspected methanol poisoning with significant
metabolic acidosts, an osmolar gap greater than 10 mosm/L, or a measured
serum methanol concentration greater than 40 mg/dL Dialysis should be
continued until the methanol concentration is less than 20 mg/dL Note: The
ethanol infusion must be increased during dialysis (see p312).

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