Multiple drugs overdose

Abstract

A 64-year-old man developed cardiogenic shock, sinus bradycardia, hypotension, lactic acidosis, hypoxic-ischaemic brain injury, polyneuropathy, renal failure and cognitive impairment [not all outcomes stated] following an intentional overdose of nimodipine, metformin, risperidone, pravastatin and ranitidine [routes not stated]. The man, presented to hospital following an intentional ingestion of nimodipine 840mg, risperidone 88mg, metformin 42g, ranitidine 9g and pravastatin 840mg in an overdose. He was involved in an argument with his neighbour before the overdose, and called the ambulance himself. Upon arrival, he showed a patent airway and was conversing. However, he was in extreme cardiogenic shock with sustained sinus bradycardia at 50 beats/minute and systolic BP of 45mm Hg. His Glasgow Coma Scale was 15/15. He had a glucose level of 11.9 mmol/L and a rectal temperature of 32.4°C. Initial arterial blood gas showed a pH of 7.01, paO2 of 47.6 kPa, paCO2 of 3.3 kPa, base excess-24.8 mmol/L and lactate 17 mmol/L. His osmol gap, calculated from serum osmolality-calculated osmolality [2(Na + + K +)+glucose + urea] was 10.5 mOsm/kg H2O. The man was resuscitated along with peripheral ephedrine, atropine and normal saline. A central venous catheter and an arterial line were sited. Subsequently, epinephrine and dobutamine infusions were initiated. Additionally, he received calcium gluconate and glucagon followed by a lipid emulsion and sodium bicarbonate. However, he remained persistently hypotensive and bradycardic. Subsequently, he was started on hyperinsulinaemia/euglycaemia therapy. He received dextrose, followed by short-acting insulin and insulin maintenance. Repeated investigations showed a pH of 6.93, paO2 of 42.9 kPa, p2CO2 of 5.4 kPA, a base excess-23.8 mmol/L and lactic acidosis of more than 20 mmol/L; his blood gas values had not improved. He was intubated and treated with propofol and atracurium besilate. Veno-arterial extracorporeal membrane oxygenation (VA-ECMO) was performed in the emergency department, 4 hours into the resuscitative effort. Afterwards, he was transferred to the ECMO centre. He was treated with methylene blue infusion. Five days after his initial presentation, he was de-cannulated and weaned off ECMO. After 11 days, he was ex-tubated. A CT scan showed sustained hypoxic-ischaemic brain injury with multiple white matter infarcts. He required critical care for polyneuropathy and dialysis for renal failure. Four months following the overdose, he remained in an inpatient ward with cerebral performance category 3. He showed mild cognitive impairment; however, he was able to perform some activities of daily living independently. He also communicated his needs and thoughts. He did not require respiratory or cardiovascular support and underwent physical rehabilitation, awaiting placement [not all outcomes stated].

Full text

Reactions 1721, p202 - 29 Sep 2018
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Multiple drugs overdose
Various toxicities: case report
A 64-year-old man developed cardiogenic shock, sinus
bradycardia, hypotension, lactic acidosis, hypoxic-ischaemic
brain injury, polyneuropathy, renal failure and cognitive
impairment [not all outcomes stated] following an intentional
overdose of nimodipine, metformin, risperidone, pravastatin
and ranitidine [routes not stated].
The man, presented to hospital following an intentional
ingestion of nimodipine 840mg, risperidone 88mg, metformin
42g, ranitidine 9g and pravastatin 840mg in an overdose. He
was involved in an argument with his neighbour before the
overdose, and called the ambulance himself. Upon arrival, he
showed a patent airway and was conversing. However, he was
in extreme cardiogenic shock with sustained sinus bradycardia
at 50 beats/minute and systolic BP of 45mm Hg. His Glasgow
Coma Scale was 15/15. He had a glucose level of 11.9 mmol/L
and a rectal temperature of 32.4°C. Initial arterial blood gas
showed a pH of 7.01, paO2 of 47.6 kPa, paCO2 of 3.3 kPa, base
excess –24.8 mmol/L and lactate 17 mmol/L. His osmol gap,
calculated from serum osmolality–calculated osmolality
[2(Na+ + K+)+glucose + urea] was 10.5 mOsm/kg H2O.
The man was resuscitated along with peripheral ephedrine,
atropine and normal saline. A central venous catheter and an
arterial line were sited. Subsequently, epinephrine and
dobutamine infusions were initiated. Additionally, he received
calcium gluconate and glucagon followed by a lipid emulsion
and sodium bicarbonate. However, he remained persistently
hypotensive and bradycardic. Subsequently, he was started on
hyperinsulinaemia/euglycaemia therapy. He received
dextrose, followed by short-acting insulin and insulin
maintenance. Repeated investigations showed a pH of 6.93,
paO2 of 42.9 kPa, p2CO2 of 5.4 kPA, a base excess
–23.8 mmol/L and lactic acidosis of more than 20 mmol/L; his
blood gas values had not improved. He was intubated and
treated with propofol and atracurium besilate. Veno-arterial
extracorporeal membrane oxygenation (VA-ECMO) was
performed in the emergency department, 4 hours into the
resuscitative effort. Afterwards, he was transferred to the
ECMO centre. He was treated with methylene blue infusion.
Five days after his initial presentation, he was de-cannulated
and weaned off ECMO. After 11 days, he was ex-tubated. A CT
scan showed sustained hypoxic-ischaemic brain injury with
multiple white matter infarcts. He required critical care for
polyneuropathy and dialysis for renal failure. Four months
following the overdose, he remained in an inpatient ward with
cerebral performance category 3. He showed mild cognitive
impairment; however, he was able to perform some activities
of daily living independently. He also communicated his needs
and thoughts. He did not require respiratory or cardiovascular
support and underwent physical rehabilitation, awaiting
placement [not all outcomes stated].
Author comment: "A 64-year-old man presented to a
district hospital following an intentional overdose of
nimodipine 840 mg, metformin 42 g, risperidone 88 mg,
pravastatin 840 mg and ranitidine 9 g." "Cardiovascular
instability associated with calcium channel blocker toxicity
comprises a small percentage of overdose presentations, yet
they are associated with a high mortality rate."
Fadhlillah F, et al. Pharmacological and mechanical management of calcium
channel blocker toxicity. BMJ Case Reports 2018: 225324, 2018. Available from:
URL: http://doi.org/10.1136/bcr-2018-225324 - United Kingdom 803346307
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