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38 CASE 38


A 17-year-old man is brought to the emergency department by his coworkers because of “abnormal behavior.”


The patient is working for the summer in a plastics factory. He has been working there for 1 month, but today he appeared confused, sleepy, and complained of dizziness and headaches.



PHYSICAL EXAMINATION



VS: T 37°C, P 120/min, R 30/min and shallow, BP 100/90 mm Hg

PE: Skin appears unusually pink. Retinal arteries and veins both appear pink. Patient’s mental status is confused and lethargic. He appears weak from a loss of muscle strength. A bitter almond smell is detected on the patient’s breath.


LABORATORY STUDIES



Arterial blood gases: PO2 105 mm Hg, PCO2 18 mm Hg, pH 7.32, wide anion gap

Pulse oximetry: 98%

Mixed venous blood gases: PO2 60 mm Hg, PCO2 20 mm Hg, pH 7.30

Plasma lactate concentration: Elevated 18 mmol/L

Plasma analysis: Cyanide


DIAGNOSIS


Cyanide poisoning



PATHOPHYSIOLOGY OF KEY SYMPTOMS


Cyanide is used in the manufacture of plastics, pesticides, and photographic materials and, therefore, cyanide poisoning can occur in the factory setting. Cyanide poisons the mitochondria by binding to cytochrome oxidase, uncoupling the oxidative phosphorylation pathway by preventing electron transport. The mitochondria can no longer produce adenosine triphosphate (ATP), and the symptoms match those characteristic of other forms of hypoxia. One difference is the arterial blood gases in this case will show elevated PO2 (because the body in not using it for metabolism) and diminished PCO2 (because little is being produced). The mixed venous blood gases show an elevated O2 because tissue extraction of O2 is greatly diminished.


The diminished ATP production affects all organ systems, but the central nervous system is the primary target of cyanide toxicity. The impaired neuronal function results in altered mental status, including confusion, lethargy, dizziness, and headache. Higher concentrations of cyanide can result in convulsion, coma, and death. Diminished ATP availability to the skeletal muscle also results in muscle weakness.


Mixed venous blood PO2 is elevated, and PCO2 is low, owing to the lack of aerobic metabolism in the tissues. Arterial blood gas values show slightly elevated PO2, reflecting a slight increase in alveolar PO2 due to the fall in PCO2. The arterial blood gas sample also shows diminished PCO2, reflecting both the low PCO2 of the blood entering the lungs and the small CO2 exchange at the lungs.


The patient has a high respiratory rate from hypoxic stimulation of the arterial chemoreceptors. The arterial PO2 is elevated, but the arterial chemoreceptors have to metabolize oxygen to sense PO2 levels. Consequently, the cyanide disruption in chemoreceptor metabolism results in the chemoreceptor determination of hypoxia. Arterial CO2 levels are low and thus do not contribute to the ventilatory drive that occurs after cyanide poisoning.


The patient exhibits a mild acidosis because anaerobic metabolism (lactic acidosis) is used as the remaining route for ATP production.

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Jul 4, 2016 | Posted by in PHYSIOLOGY | Comments Off on 38

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