Fig. 2.1
Chest x-ray on admission to accident and emergency
ECG: rate 50/min regular, flat T waves in III, AVF, V4–6.
Urgent CT-head, no abnormality detected.
Comment on Her FBC
This lady has anaemia with normal WBC and platelet counts She has raised MCV and therefore the differential diagnosis for her anaemia includes:
Alcohol
Vitamin B12 or folate deficiency
Myelodysplasia
Hypothyroidism
Haemolytic anaemia
Drugs: particularly those interfering with DNA synthesis such as Azathioprine, methotrexate, Zidovudine
Aplastic anaemia
Acquired sideroblastic anaemia
However, the mild abnormality in her FBC is unlikely to have contributed to the clinical presentation.
Comment on Her U&Es
This lady has hyponatraemia and raised bicarbonate. The commonest cause of low sodium is the use diuretics, some of which can also cause metabolic alkalosis. This patient is on bendrofluazide, which may have caused this abnormality although there are other possibilities (for full review of hyponatraemia, please see Case 10). The modest drop in her sodium is unlikely to be the cause for her presentation.
Comment on the CXR
The heart shows significant enlargement and there is a mild degree of pleural effusion, more evident on the left. There are no clear signs of heart failure in the lung fields and therefore the enlarged globular heart does not necessarily represent dilated cardiac chambers and more likely to be due to pericardial effusion.
How would you proceed in this patient?
There are few clues in the history to point towards a clear diagnosis. In a situation like this, it is helpful to make a list of the main abnormalities to try to reach the right diagnosis.
Admission: collapse and drop in GCS.
History: memory problems and behavioural issues with a family history of autoimmunity.
Investigations: decompensated respiratory acidosis (raised bicarbonate may be a marker of chronic metabolic alkalosis). Large heart on CXR and non-specific ECG abnormalities.
Focussing further on one serious abnormality likely to be the cause of her clinical presentation, respiratory acidosis is a clear culprit.
What is the differential diagnosis of respiratory acidosis?
This includes:
Lung pathology: COAD is a potential cause in our patient but normal chest auscultation and clear lung fields argue against this being the main cause of the symptoms.
Central nervous system pathology: The failure to detect neurological signs and normal CT head makes this an unlikely diagnosis. Central hypoventilation may occur secondary to opioid use. Our patient has osteoarthritis and may have been prescribed additional pain killers. Therefore, a careful drug history from the GP is mandatory. Normal pupils that are reactive to light effectively rules out this possibility but checking with the GP is still recommended. In cases of doubt, naloxone can be administered to reverse the action of any opioid. Finally, endocrine disorders such as hypothyroidism may cause hypoventilation but there is no history of a thyroid disorder in our patient.
Neuromuscular disease: This includes myasthenia gravis, Guillain-Barré and amyotrophcic lateral sclerosis. These conditions are not consistent with the history of the presentation or patient examination.
Obesity-hypoventilation: this can occur in individuals with significant weight problems (see Case 10), but our patient had a weight of 69 kg with a BMI of 25.7 kg/m2, making this an unlikely diagnosis.
The patient deteriorates over the next few hours and her GCS drops to 9/15. Repeat blood gas analysis shows a rise in pCO2 to 9.1 kPas and a drop in pH to 7.19. What would you do?
Summarising the major abnormalities, the patient has a central hypoventilation disorder together with an enlarged heart on CXR and a small pleural effusion. The GP cannot be reached and therefore a trial with naloxone is not unreasonable.
The patient is given naloxone, but no change in her condition is noted. Would you request thyroid function tests at this stage?
Thyroid tests should NOT be generally requested in patients who are ill and the only exception is when it is thought the illness is directly related to thyroid dysfunction. Therefore, it is important to undertake an examination of the thyroid status and palpate the neck followed by requesting thyroid function tests.
On examination, the patient is noted to have a dry skin but there are no other convincing signs of hypothyroidism. One doctor reports slow relaxation of ankle reflexes, whereas another, who is more senior, disagrees. Neck palpation is unremarkable. Her TFTs show:
FT4: 1.1 pmol/L (normal 10–20)
TSH: 97 mIU/L (normal 0.2–4.5 mIU/L)
Does this patient have hypothyroidism, or are these abnormal TFTs related to euthyroid sick syndrome (ESS)?
In ESS, T3 levels are typically low and in more advanced cases T4 levels can fall, whereas TSH is normal or low normal [1, 2]. TSH levels can marginally rise, particularly as the acute illness is brought under control, but these never reach the levels seen in our patient. Therefore, our diagnosis fits with primary hypothyroidism [3, 4]. Positive thyroid peroxidase antibodies will confirm the autoimmune nature of hypothyroidism and it is a test worth requesting.
Does primary hypothyroidism offer a unifying diagnosis for the symptoms and signs in our patient?
Primary hypothyroidism can cause memory loss and alter behaviour. Dry skin and bradycardia are classical signs of hypothyroidism [5, 6]. Low thyroid hormones can result in hyponatraemia and non-specific ST-T segment changes on ECG. Mild anaemia with raised MCV is seen with hypothyroidism whereas pericardial and pleural effusions are known to occur, particularly in severe thyroid hormone deficiency. Respiratory acidosis is one of the criteria to diagnose myxoedema coma and therefore the likely unifying diagnosis in our patient is hypothyroidism causing myxoedema coma.
The criteria used to diagnose myxoedema coma can vary greatly and recent work attempted to diagnose this condition using a scoring system that includes alteration in thermoregulation, central nervous, cardiovascular, gastrointestinal and metabolic systems with and without a precipitating event [7]. Even using this system, some cases can be missed and therefore the diagnosis requires a high degree of suspicion and appropriate expertise.
What would you do in this patient?
This patient, with a diagnosis of myxoedema coma, should be managed in intensive care setting as she can deteriorate quickly (mortality is up to 50 %, although this is now on the decrease) [8].
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