Acute cyanide poisoning complicated by lactic acidosis and pulmonary edema

Cyanide poisoning via the oral route is a remarkably rare entity in the United States. Though acute toxicity from this poison may present with classic signs and symptoms (smell of bitter almonds on breath and cherry-red skin), these signs are frequently not clinically observed in the intoxicated patient, making it low on the routine differential diagnosis leading to both diagnostic and therapeutic challenges for the bedside clinician. This is a case of a 17-yearold male with a history of depression who presented to the Emergency Room (ER) with altered mental status, abdominal pain, and emesis. A severely elevated and worrisome lactic acidosis triggered the ER’s septic shock bundle and algorithm, but further investigation ultimately led to the unifying diagnosis of intentional cyanide poisoning.

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Value of lactic acidosis in the assessment of the severity of acute cyanide poisoning

Critical Care Medicine ◽

10.1097/00003246-200209000-00015 ◽

2002 ◽

Vol 30 (9) ◽

pp. 2044-2050 ◽

Cited By ~ 126

Author(s):

Frédéric J. Baud ◽

Stephen W. Borron ◽

Bruno Mégarbane ◽

Hervé Trout ◽

Frédéric Lapostolle ◽

...

Keyword(s):

Lactic Acidosis ◽

Cyanide Poisoning

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Fatality from potassium gold cyanide poisoning

BMJ Case Reports ◽

10.1136/bcr-2019-229947 ◽

2019 ◽

Vol 12 (7) ◽

pp. e229947 ◽

Cited By ~ 1

Author(s):

Elizabeth Harmon ◽

Jacob Lebin ◽

David Murphy ◽

Bjorn Watsjold

Keyword(s):

Lactic Acidosis ◽

Potassium Cyanide ◽

Clinical Findings ◽

Rapid Decline ◽

Gold Cyanide ◽

Cyanide Poisoning ◽

Severe Lactic Acidosis ◽

Cyanide Toxicity ◽

Intentional Ingestion ◽

Antidotal Therapy

While potassium cyanide poisoning has been well described, the toxicity of potassium gold cyanide is less well understood. This case describes an 84-year-old man who presented after an intentional ingestion of 0.5–1 teaspoons of potassium gold cyanide. Despite antidotal therapy, the patient rapidly developed severe lactic acidosis, multiorgan dysfunction and ultimately expired. While the patient’s clinical findings were consistent with acute cyanide poisoning, a serum cyanide level was below the toxic threshold. Previous reports have suggested that gold toxicity may also contribute to the effects of potassium gold cyanide, and may have played a role in the patient’s rapid decline. In addition to treatment of cyanide toxicity, management of acute gold toxicity should also be considered in potassium gold cyanide ingestion.

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An unusual cause of severe lactic acidosis: cyanide poisoning after bitter almond ingestion

Intensive Care Medicine ◽

10.1007/s00134-010-2029-8 ◽

2010 ◽

Vol 37 (1) ◽

pp. 168-169 ◽

Cited By ~ 17

Author(s):

Pascale Sanchez-Verlaan ◽

Thomas Geeraerts ◽

Sophie Buys ◽

Béatrice Riu-Poulenc ◽

Claudine Cabot ◽

...

Keyword(s):

Lactic Acidosis ◽

Cyanide Poisoning ◽

Severe Lactic Acidosis ◽

Bitter Almond

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Pulmonary Edema and Simultaneous Cardiac Dysfunction After Epileptic Seizures

Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques ◽

10.1017/s0317167100017911 ◽

2013 ◽

Vol 40 (06) ◽

pp. 896-897

Author(s):

V. Pelliccia ◽

C. Pizzanelli ◽

S. Pini ◽

P. Malacarne ◽

U. Bonuccelli

Keyword(s):

Pulmonary Edema ◽

Cardiac Dysfunction ◽

Epileptic Seizures

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Oxygen radicals participate in alloxan-induced pulmonary EDEMA

Proceedings, annual meeting, Electron Microscopy Society of America ◽

10.1017/s0424820100159047 ◽

1990 ◽

Vol 48 (3) ◽

pp. 298-299

Author(s):

Tomoo Kawada ◽

Michio Arakawa ◽

Kenjiro Kambara ◽

Takashi Segawa ◽

Fumio Ando ◽

...

Keyword(s):

Pulmonary Edema ◽

Oxygen Radicals ◽

Bolus Injection ◽

Physiological Saline ◽

Baseline Period ◽

Alveolar Epithelial Cells ◽

Control Group ◽

Intervention Period ◽

Lung Water ◽

Electron Microscopic

We know that alloxan causes increased-permeability pulmonary edema and that alloxan generates oxygen radicals (H2O2, O2−, ·OH) in blood. Therefore, we hypothesize that alloxan-generated oxygen radicals damage pulmonary capillary endothelial cells, and, possibly, alveolar epithelial cells as well. We examined whether oxygen radical scavengers, such as catalase or dimethylsulfoxide (DMSO), protected against alloxaninduced pulmonary edema.Five dogs in each following group were anesthetized: control group: physiological saline (20ml/kg/h); alloxan group: physiological saline + alloxan (75mg/kg) bolus injection at the beginning of the experiment; catalase group: physiological saline + catalase (150,000u/kg) bolus injection before injection of alloxan; DMSO group: physiological saline + DMSO (0.4mg/kg) bolus injection before alloxan. All dogs had 30-min baseline period and 3-h intervention period. Hemodynamics and circulating substances were measured at the specific points of time. At the end of intervention period, the dogs were killed and had the lungs removed for electron microscopic study and lung water measurement with direct destructive method.

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