Lab Case 230 interpretation

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Question 1 answer:

Ph = 7.38, PCO2 = 43 and HCO3 = 25.3. These levels are all within acceptable levels for venous blood gas. SO, we have normal blood gases balance.

COHb = 35 (usual level is up to 4% in non-smokers and up to 10% in heavy smokers). So we have moderate to severe carboxyhaemoglobinaemia.

K = 2.5, that is moderate hypokalemia

Lactate = 3.8, that is lactosis.

Na, Cl, MetHb, Cr and glucose are with in normal ranges.

So final conclusion is moderate to severe carboxyhamoglobinaemia with associated moderate hypokalaemia and lactosis.

 

 Question 2 Answer: 

Causes of Carboxyhaemoglobinaemia:

  • Exposure to environmental carbon-monoxide
  • Haemolytic anaemia (Carbon monoxide is produced in a small amount as a byproduct of haem catabolism).

Causes of Hypokalaemia:

In general, hypokalaemia can happen due to potassium loss (either through GI tract or urinary system) or due to intracellular shift.

Factors that will increase intracellular K shift and reduce plasma potassium levels:

  • Insulin
  • Beta-adrenergic agents
  • Alkalosis (increased PH).

Carbon monoxide poisoning (Carboxyhaemoglobinaemia) will result in impaired glucose sensing. The brainstem and the hypothalamus have glucose-sensing or glucose-inhibiting neurons, which can control the autonomic nervous system and affect the metabolic state of the liver, muscles, and fat tissue and the secretory function of the pancreas. This results in increase glucose production and reduced insulin secretion.

After treatment of CO poisoning, the glucose sensing centres will start to function again resulting in insulin secretion. Lowering of the hyperglycemia that is associated with severe CO poisoning will result in shift of K to the intracellular compartment and that results in hypokalaemia.

 

 Causes of lactosis:

The cause of elevated lactate level in this case can be attributed to CO poisoning or due the seizure that she suffered.

elevation of lactate level is an indication of the severity of CO poisoning. CO has 210-fold more affinity for hemoglobin compared with oxygen. Accordingly, when CO and oxygen compete to bind to hemoglobin, CO wins the contest. Therefore, even small increase in CO level may cause poisoning. This high affinity also impairs the delivery of O2 to the cells resulting in tissue hypoxia and shifting of the oxygen-hemoglobin dissociation curve to the left. Tissue will rely on anaerobic metabolism and that will produce lactosis.

High lactate after seizure activity is due to local muscle hypoxia during the seizures. Although these changes can be quite marked, the condition is self-limiting and usually does not call for any specific treatment.

 *** If lactate level is more than 10 in patient with monoxide poisoning – especially if the poisoning is due to burn in a closed place – we need to consider cyanide toxicity as a possible additional diagnosis.

 

Question 3 answer: 

Every patient with suspected CO toxicity should get blood gases checked, this will show the carboxyhaemoglobin level. This will confirm the diagnosis and will determine the severity – COHb level correlate with the symptoms.

ECG should be performed to exclude ischemia (as part of generalized tissue hypoxia).  Female patients should get BHCG level checked.

After securing AB and C, these patients need high – flow – Oxygen as soon as possible. all patients should receive 100% oxygen until symptoms have resolved. Pregnant patients should receive 100% oxygen for 24 hours.

We should consider this patient for hyperbaric O2 Therapy.

Indications of hyperbaric O2 therapy in CO poisoning:

  •  Loss of consciousness (even if it is transient).
  • Loss of vision
  • Every patient, at any age, if COHb >25–40%.
  • In patients with ischemic heart disease, if COHb >20%.
  • In children and pregnant women, if COHb >15%.
  • Signs of cardiac ischemia or arrhythmia on ECG
  • Any clinical finding persisting for 3 weeks or more.
  • Persistence of clinical symptoms despite high-flow oxygen therapy for 4 hours.

 

Hyperbaric oxygen therapy shortens half-life of COHb, reduces production and level of oxygen free radicals, inhibits lipid peroxidation, and improves impaired mitochondrial functions and platelet aggregation in capillaries.

Hyperbaric O2 therapy shortens recovery time, decrease mortality rate, and reduce the risk developing neuropsychiatric symptoms in the long term in comparison with use of normobaric oxygen therapy.