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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
showed, vital signs : blood pressure 130/80 mmHg, heart rate 88 x/minute, axillarys
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
showed, vital signs : blood pressure 130/80 mmHg, heart rate 85 x/minute, axillarys
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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