Tutorial for Trainees

A farmer with abdominal pain

Dr. C.Y. MAN

 Triage
 On stretcher
 rolling in bed with pain
 alert
 BP 160/100
 pulse 60/min
 Respiratory rate:20/min
 SaO2: 97% on room air
 afebrile
 Because of the severe pain
and cold sweating, he was
sent to the resuscitation room
What are your ddx for severe abd
pain?
What would you like to know from the
patient’s wife?
 History
 A 56 years old farmer who lives in farm
near the border with the mainland china
 while working one day in the field spraying
the crops and weeding out wild growth
 complains of sudden onset of abdominal
pain with an urge to defecation
 the pain was so severe that he had to stop
working and call the ambulance
 Further history
 There was nausea but no vomiting
 He felt a bit short of breath
 cold sweating noted
 denied chest pain
 took lunch 2 hours ago with wife who was
looking well
 Further history
 denied taking any medications
 past health was good all along except for hy
pertension taking regular natrilix from GOP
D for 10 years

What are your ddx at this point.

 Examination
 Vital signs as above
– BP 160/100
– pulse 60/min
– Respiratory rate:20/min
– SaO2: 97% on room air
 GCS 15/15
 Obvious distress due to pain
 Examination (cont’d)
 Abdomen was soft, but diffusely tender to t
ouch. No guarding or rebound was elicited.
 No organomegaly or abnormal mass was de
tected
 The bowel sound was active
 PR was empty
 Examination (cont’d)
 Chest showed mild rhonchi bilaterally
 Heart sounds were normal, with no murmur
heard

Any other physical findings you would like to know?

 Additional findings

 pupils 2 mm in diameter, equal and reactive

to light
 no weakness noted
What is the likely cause of his
abdominal pain?
Bowel Colic
A dose of buscopan 40 mg wa
s given but without significant i
mprovement
What would you do now?

Reassess patient.
Investigations?
 Bedside Investigations
 Haemoglobin 14 g/dL
 Haemoglucostix 6 mmol/L
 Arterial blood gases (15 L/min O2):
 pH 7.33, PCO2 4 kPa,, PO2 30 kPa, HCO3
26 mmol/l
 amylase normal
 CXR and AXR were both unremarkable
The patient had evidence of br
onchospasm with mild shortne
ss of breath and rhonchi on th
e chest. Does that give any cl
ue to the cause of his bowel c
olic?
The cause of his bowel colic
might have also caused the
bronchospasm. What
common pharmacological
properties was there in
action?
Cholinergic activities. The pati
ent was under excessive choli
nergic activity. If the patient h
as been poisoned, name one l
ikely poison with such activity.
Organophosphate poisoning
Indeed, the patient had been spraying
the crops with an organosphosphate i
nsecticide bought from mainland Chi
na. But he denied ingesting any of it.
How can the insecticide get
into his body to cause
toxicity?
Organosphophate can get into
the body through the skin and
by inhalation. It is likely that h
e was poisoned in such ways.
 Knowing the absorption
properties of the poison, what
additional procedures should
have been carried out as soon
as the patient presented?
 All attending staff should put
on personal protection
equipment and all the clothes
of the patient should be
removed immediately and the
skin decontaminated.
What are the antidotes for ora
gnosphosphate poisoning?
 Antidote
 Atropine
– a competitive antagonist to acetylcholine
– large total doses may be necessary
 pralidoxime
– regenerate cholinesterase from cholinesterase-o
rganophosphate complex
 Outcome
 Atropine were started at AED and continue
d after admission
 Patient’s skin was decontaminated
 admitted to ICU for possible respiratory fail
ure
 symptoms gradually improved with repeate
d doses of atropine and pralidoxime
 plasma cholinesterase level found to be low
Diagnosis: organophosphate
poisoning
What are the toxic effects of
organophosphate poisoning?
SLUDGE (muscarinic effects)
 Salivation
 Lacrimation
 Urination
 Defecation
 Gastrointestinal distress
 Emesis
 Nicotinic effects
 Fasciculation  hypertension
 cramping  tachycardia
 weakness->paralysis-  dilated pupils
>respiratory failure  pallor
 areflexia
 CNS effects
 Restlessness  Generalized weakness
 emotional lability  delirium
 headache  psychosis
 tremor  coma
 drowsiness  seizures
 confusion  cardiorespiratory depr
 slurred speech ession
 ataxia  death
 Learning points
 Patient can still be poisoned without a history of to
xic ingestion
 organophosphate can be absorbed through the skin
and by inhalation
 skin decontamination and personal protection mus
t be carried out for possible organophosphate pois
oning
 depending on severity, full-blown toxidrome does
not necessarily occur in real situation