From the reading I just did, it sounds like a horrible death.
Early
symptoms include nausea, vomiting,
retrosternal and epigastric pain, dyspnea,
anxious, agitation and smell of garlic [22,
23, 24]. On the breath. Moreover shock and
peripheral circulatory failure are mainly
imperative early signs of toxicity.
Cardiac toxicity
Cardiac toxicity comprises circulatory
failure hypotension [26, 27, 28], congestion
of the heart, separation of myocardial fibres
by edema, fragmentation of fibres, non-
specifc vacuolation of myocytes, focal
necrosis, neutrophil and eosinophil
infiltration were found in autopsy [29-32].
Also, significantly increasing left ventricular
dimensions [33], hypokinesia of the left
ventricle and septum, akinesia, ejection
fractions reduction [34], severe hypotension,
raised systemic venous pressure, normal
pulmonary artery wedge pressure,
inadequate systemic vasoconstriction and
ECG abnormalities (ST and T-wave
changes) are other signs and symptoms.
Respiratory toxicity
Tachypnea, dyspnea, crepitations, and
rhonchi were present on examination in 192
out of 418 cases (46%) of phosphide
poisoning [31], and have been found by
others [36].Pulmonary edema is common
but it is not always clear whether it is
cardiogenic or non-cardiogenic in etiology.
It tends to develop 4–48 h after ingestion
and the finding of a reduced arterial pressure
of O2 without an increase in pulmonary
artery wedge pressure, suggested it was non-
cardiogenic [35]. Others have confidently
diagnosed adult respiratory distress
syndrome [25, 33, 37, 38], and non-specifed
pulmonary edema [39,40]. The edema fluid
may be protein-rich and hemorrhagic.
Gastrointestinal toxicity
Hematemesis [36], corrosive lesions of the
esophagus and stomach [41, 42], vomiting,
epigastric pain, severe gastric erosions,
duodenal erosions, esophageal strictures
tracheo-oesophageal fistulae,dysphagia.
Dysphagia may be apparent as soon as 3 or
4 days after ingestion of aluminium
phosphide but is more usual about 2 weeks
later.
Hepatic toxicity
Transient elevations of alanine
aminotransferase and aspartate
aminotransferase activities are not
infrequent after ingestion of metal
phosphides [44-47], but jaundice secondary
to liver damage is much less common [39].
It was present in 12 out of 92 cases (Singh,
et al, 1991) and was said to be common in
another series of 15 patients [48], but
confirmatory laboratory data were not
provided. Jaundice was alleged to be present
in 16 (52%) members of the crew of a grain
freighter who inhaled phosphine after an
accidental release [49], but, in the six tested,
serum bilirubin concentrations were normal
and transaminase activities only minimally
disturbed, casting doubt on the clinical
observation. Acute hepatic failure and
encephalopathy was considered to be the
cause of death in one man [50], while a 12-
yearold girl died from a combination of
acute hepatic failure and encephalopathy
with renal failure [27]. Portal edema,
congestion of the portal tract and central
veins, and vacuolization of hepatocytes are
the most frequent findings at autopsy.