A Patient With Puffer Fish Poisining

8/4/2019 A Patient With Puffer Fish Poisining

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isochors pupil with 5 mm in diameter and positive light reflex; chest : symmetric, no

retraction, heart : single and reguler of 1st and 2nd heart sound, no murmurs, no

gallops, no extra systole; lung : vesicular, no wheezing, no ronchy; abdomen :

unpalpable liver and spleen, normal intestinal sound, no meteorism, no ascites;

extremities : warm, clammy, mild parese in leg, normal physiologic reflex, no

abnormal reflex.

Laboratory findings were : Hb 10,9 g/dl, Leuc 5,8 x 109/L, Thromb 221x 109/L,

PCV 0,32, randomised blood sugar 149 mg/dl, creatinin serum 0,9 mg/dl, BUN 18

mg/dl, AST 56,4 U/L, ALT 34,3 U/L, K serum 3,5 meq/L, Na serum 139 meq/L, blood

gas analysis Ph 7,39, pCO2 32,6 mmHg, pO2 77,8 mmHg, HCO3 19,4 mmol/L, BE

5,6, O2 saturation 95,6 %. Chest photo was with normal limit. ECG tracing showed

sinus tachycardia 107 x/minute, normal axis.

Based those data, we assessed the patient with puffer fish poisoning with

hypoxemia. The treatments were secure arway, oxygenation with nasal prong 2

L/minute, Ringer Lactate infusion 2.000 cc/24 hour, perform NG tube and then gastric

washing, norit 50 g, neostigmin 0,1 mg intramuscularly. Monitoring closely was

performed to vital sign, ECG, clinical manifestasion.

CLINICAL COURSE

First Day 7.30 pm

The patient was apnea suddenly and unconscious. Physical examination

showed, vital sign : blood pressure 120/80 mmHg, heart rate 104 x/minute, axillarys

temperature 37,50C, apnea, GCS 112; head and neck : pupil 7 mm in diameter,

corneal and light reflex was weak positive, hypersalivation; chest : simetric, apnea;

heart : normal heart sound, regular, no extrasystole-murmur-gallop; lung : apnea;

abdomen : liver and spleen was unpalpable, decreased intestinal sound; extremity :

paresis, decreased physiologic reflex, there was no pathologic reflex. The

assessment was puffer fish poisoning with apnea, paresis and decreased physiologic

reflex. The treatment was intubations and performing respirator, the others were

same as before.

Second Day 6.00 am

Patient was in deep coma, still performing respirator. Physical examination

showed, vital signs : blood pressure 130/85 mmHg, heart rate 103 x/minute, axillarys


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temperature 37,50C, respiration rate 20 x/minute, GCS 111; head and neck : pupil 7

8 mm in diameter, corneal light-oculomotor-gauge-nystagmus reflex was negative,

hypersalivation; chest : simetric; heart : normal heart sound, regular,no extrasystole-

murmur-gallop; lung : vesicular, no ronchy and wheezing; abdomen : liver and spleen

was unpalpable, decreased intestinal sounds; extremity : flaccid, there was no

physiologix reflex and pathologic reflex. Blood gas analysis Ph 7,32, pCO2 46,8

mmHg, pO2 241,7 mmHg, HCO3 23,7 mmol/L, BE -2,4, O2 saturation 99,5 %.

Concultation to neurology department : unconciousness with negative brainstem

reflex. The assessment was puffer fish poisoning with apnea, paralysis and negative

brain stem reflex, slightly combined respiratory and metabolic acidosis. The

treatment was intubation and performing respirator, iv RD5 : D10 = 1.000 cc : 1.000

cc, iv ranitidin 1 amp q12h, im neostigmin 0,1 mg q6h.

Second Day 01.00 pm

Patient was conscious, breathing spontaneously. Physical examination


temperature 37,50C, respiration rate 20 x/minute, GCS 456; head and neck : pupil 5

mm in diameter, corneal light-oculomotor-gauge-nystagmus reflex was positive;

chest : simetric; heart : normal heart sound, regular,no extrasystole-murmur-gallop;

lung : vesicular, no ronchy and wheezing; abdomen : liver and spleen was

unpalpable, normal intestinal sounds; extremity : no paresis, there was normal

physiologix reflex and no pathologic reflex. Blood gas analysis Ph 7,35, pCO2 42,6

mmHg, pO2 181 mmHg, HCO3 23,1 mmol/L, BE -2,5, O2 saturation 99,2 %. The

assessment was puffer fish poisoning and getting better. The treatment was

extubation, enteral diets 200cc q8h, iv RD5 : D10 = 1.000 cc : 1.000 cc, iv ranitidin 1

amp q12h, im neostigmin 0,1 mg q6h. The patient was referred to intermediate ward.

Seventh Day 07.00 am

Patient was conscious, breathing spontaneously. Physical examination


temperature 370C, respiration rate 20 x/minute, GCS 456; head and neck : pupil 5

mm in diameter, corneal light-oculomotor-gauge-nystagmus reflex was positive;

chest : simetric; heart : normal heart sound, regular,no extrasystole-murmur-gallop;

lung : vesicular, no ronchy and wheezing; abdomen : liver and spleen was

unpalpable, normal intestinal sounds; extremity : no paresis, there was normalphysiologix reflex and no pathologic reflex. The assessment was post puffer fish


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poisoning. The treatment was high calories (2.100 cal) and high protein (2g/kgbw)

diets orally, iv RL 1.000 cc, tab ranitidin 150 mg q12h, neostigmin was discontinued.

The patient was referred to male tropical ward.

Tenth Day 11.00 am

The patient was discharged.

DISCUSSION

Puffer fish/ fugu/ buntek fish/ blow fish/ globe fish/ swell fish was included

famili tetraodontidae, class osteichthyes, orde tetraodontiformes. This genus consist

of about 100 species. Puffer fish have short and globe body with 40 cm in lenght, the

skin is hard with soft burr. Puffer fish can swell it self if in threatening condition or on

land by swallowing a lot of water or air as seen in figure 1. Puffer fish contain

tetrodotoxin, a hightly potent and lethal toxin. Tetrodotoxin is concentrated in the skin

and viscera, especially in the liver and the gonads. Lesser amount of toxin may be

found in muscles. Poisoning usually occur after eating fish caught and prepared by

uncertified handlers. The toxic dose is not clear because puffer fish have different

concentrations of tetrodotoxin. The level of toxicity is seasonal, and, in Japan, fugu is

served only from October throug March. A dose of 1 2 mg of purified toxincan be

lethal. Reported cases from the Centers for Disease Control and Prevention (CDC)

have documented toxicity with ingestion of as little as 1.4 ounces of puffer fish (1, 5,

7). The family of the patient told that the patient had eaten buntek fish that

match to the characteristic of puffer fish. The fist was caugh and prepared by

the patient. The patient ate the skin and muscles of puffer fish.

Figure 1. Chemical structures of tetrodotoxin and Puffer fish.


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Tetrodotoxin is aminoperhydroquinazolone, a heat-stable, water-soluble

compound. Tetrodotoxin is a heterocyclic, small, organic molecule (as shown on

figure 1) that acts directly on the electrically active sodium channel in nerve tissue.

Tetrodotoxin blocks diffusion of sodium through the sodium channel (as shown in

figure 2), preventing depolarization and propagadation of action petentials in nerve

cell. All of the observed toxicity is secondary to the action potential blockade.

Tetrodotoxin acts on the central and the peripheral nervous systems (ie, autonomic,

motor, sensory nerves). Tetrodotoxin also stimulates the chemoreceptor trigger zone

in the medulla oblongata and depresses the respiratory and vasomotor centers in

that area (2, 5, 8, 9, 10, 11).

The first symptoms occur 15 minutes to several hour after ingestion of

tetrodotoxin-containing food. A recent report on toxicity found that initial symptoms

may occur up to 20 hours after ingestion. Initial symptoms include lip and tongue

paresthesias, followed by facial and extremity paresthesias and numbness.

Salivation, nausea, vomiting, and diarrhea with abdominal pain develop early. Motor

dysfunction with weakness, hypoventilation (may be from dysfunction of central and

peripheral nercous systems), and speech difficulties then develop. A rapid ascending

paralysis occurs over 4 14 hours. Extremity paralysis precedes bulbar paralysis,

which is followed by respiratory muscle paralysis. Deep tendon reflexes are

preserved early in the course of paralysis. Finally, cardiac dysfunction with

hypotension and dysrhytmias (bradycardia), central nervous system (CNS)

dysfunction (eg, coma), and seizures develop. Patient with severe toxicity may have

deep coma, fixed nonreactive pupils, apnea, and loss of all brain stem reflexes.

Death can occur within 4 6 hours (2, 5, 8, 9, 12, 13). Typically, death occur from

respiratory muscle paralysis and respiratory failure. The patient had lip

paresthesias, facial and extremity paresthesias, numbness, salivation, nausea,

vomiting, and diarrhea with abdominal pain, motor dysfunction with weakness,

speech difficulties, extremity paralysis, deep coma, fixed nonreactive pupil,

apnea, and loss of all brain stem reflexes.

Figure 2. The site action of several neurotoxins in neuromuscular junction


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No spesific laboratory test that confirms tetrodotoxin ingestion exists; thus,

dietary history is key for diagnosis. Mouse bioassays for paralytic shellfish toxin (ie,

saxitoxin) exist that positive with tetrodotoxin and research chromarography

techniques, but neither are available in the acute clinical situation. Tetrodotoxin also

may be detected by fluorescent spectometry. Measure routine serum electrolytes,

calcium, magnesium, and ABGs to rule out metabolic causes of diffuse sensory and

motor neuron dysfuntion (2, 5, 8, 9). Analysis of tetrodotoxin did not performe to the

patient. Diagnosis of puffer fish poisoning was based on dietary history and

patients symptoms.

Patient with evidence of cyanosis or respiratory insuffiency should have a

chest x-ray to exclude local lung pathology (eg, aspiration pneumonia). Obtain a plain

film and upright x-ray of the abdomen in patients with persistent vomiting or severe

abdominal pain to exclude obstruction or hollow viscus perforation. Perform a CT

scan of the brain if the patient exhibits any focal neurologic dysfunction or seizures

(2, 5, 8, 9). We performed chest x-ray to the patient. We did not perform CT

scan and plain film and upright x-ray of the abdomen, because there was no

indication.

The tratment of puffer fish poisoning consist of :

Focus initially on the ABCs.

Secure the airway before frank respiratory failure or aspiration occurs.

Establish an IV early in the event acute antiarrhythmics or vasopressors are

needed.

Remove toxin from the intestinal tract by the usual toxicologic modalities. The

use of nasogastric or orogastric lavage is theoretically beneficial but can be

complicated by aspiration and damage to the esophagus. Gastric lavage with a

2 % sodium bicarbonate solution has been suggested. Removal maybe

followed by charcoal and perhaps sorbitol (50 100 g of activated charcoal in

70 % sorbitol). The administraton of activated charcoal (with or without a

cathartic) is recommended for all symptomatic patients.

Carefully monitor vital signs and oxygenation in the ED because patients can

decompensate suddenly. Treat all alterations in vital signs aggressively.


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Further treatment focuses in supporting cardiovascular function until the toxin is

eliminated from the body.

No spesific antidote has been tested in human. An animal study using

monoclonal antibodies againts tetrodotoxin has been done. Monoclonal

antibodies were shown to be life saving in the mice treated both before and

after the ingestion of a lethal dose of tetrodotoxin. Further studies are needed to

document the efficiacy in human.

In another animal study, 4-aminopyridine (a potassium channel blocker) was

used in guinea pigs intoxicated with tetrodotoxin or saxitoxin. A dramatic

improvement in respiratory, cardiac, and CNS status occurred after

administration of the drug. No human studies of this drug for use in tetrodotoxin

poisoning are in progress.

No drug has been shown to reverse the effects of tetrodotoxin poisoning.

Treatment is symptomatic. Spesific drug efficacy has only been documented

anecdotally.

Anticholinesterase drugs (eg, neostigmine) have been proposen as a treatment

option but have not been tested adequately (2, 5, 8, 9, 10, 14, 15, 16).

The treatment for the patient was : secure airway, oxygenation with nasal

prong 2 L/minute, then intubations and performing respirator when the patient

became apnea. Ringer Lactate infusion 2.000 cc/24 hour, perform NG tube and

then gastric washing, norit 50 g, neostigmin 0,1 mg intramuscularly. Monitoring

closely was performed to vital sign, ECG, clinical manifestation.

Mortality rates are difficult to establish; however, anecdotal report suggest 50

60 % mortality, even with good supportive care. Symptoms may last several days,

even in nonlethal ingestions. One report suggest that prognosis is good if the patient

survives the first 24 hours (2, 5, 8, 9 ,10). Prognosis of the patient was good,

because the patient survived in the first 24 hours.

Puffer fish poisoning can be prevented by several ways, such as : not to

comsume puffer fish, excludes the visceras skin, and gonads, cooking with baking

soda, cultivation in bacterial free pool (1, 4, 6, 10).


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SUMMARY

A 25 years old man admitted in Soetomo Hospital because of puffer pish

poisoning. The patient had lightheadness sensation, perioral parestesia, paralysis,

weakness, nausea, vomiting, abdominal pain, salivation, difficulties to speech, thendeveloped to deep coma, apnea, and lost of brainstem reflexes.

The diagnosis of puffer fish poisoning was based on dietary history and

patients symptoms. Analysis of tetrodotoxin did not performed.

The treatment for the patient was : secure airway, oxygenation woth nasal

prong 2 L/minute, then intubations and performing respirator when the patient

became apnea. Ringer Lactate infusion 2.000 cc/24 hour, perform NG tube and then

gastric washing, norit 50 g, neostigmin 0,1 mg intramuscularly.

Prognosis of the patient was good, because the patient survived in the first 24

hours and discarded on 7th of admission.

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7. Polunin I, Sharma RE, Khoo Hong Yoo (1982). Underwater life. 4th ed.

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A Patient With Puffer Fish Poisining