Z022

 

Myxoedema coma with severe hypoxia

 

E Deyab, L Lei, S Hwang, F Iqbal, R Menon, North Middlesex Hospital

 

 

Myxoedema coma is a rare but treatable endocrine emergency however it must be considered as a differential diagnosis as symptoms overlap with other much more commonly occurring critical conditions.

 

The mortality rates may be as high as 3060%, particularly with delayed treatment [1]

 

The cardiovascular manifestations in myxoedema coma tend to be especially severe and life threatening in comparison to other symptoms [2]. Early symptoms of the disease comprise bradycardia and low cardiac output due to decreased cardiac contractility.

 

Pericardial effusion may also be present in such cases due to increased vascular permeability [3].

 

Myxoedema coma can also be complicated by alveolar hypoventilation and respiratory failure. Alveolar hypoventilation occurs due to decreased ventilatory response to hypoxia and hypercapnia [4,5]. There is weakness of respiratory muscles as well as a decrease in the central drive [4,6]

 

Abstract: We report a case of a 28-year-old Polish woman, recently travelled to the UK, presented to the A&E with 3-week history of breathlessness and bilateral leg swelling. She had a history of Trisomy 21, amenorrhoea for 4 months and orthopnoea with periorbital oedema with conjunctival congestion. Saturation 70% on air, 96% on 15 liters of oxygen, heart rate 42, blood pressure 103/61, temperature 36.2. 

 

Investigations and management: Echocardiogram showed 3.3cm pericardial effusion, low voltage ECG and tests showed TSH >100mIU/L (0.4 4.4) with FT4 0.05pmol/L (12-22). She initially had type 1 respiratory failure and required intubation and ventilation. Pericardial effusion was drained twice. She was treated with intravenous liothyronine and hydrocortisone along with levothyroxine via nasogastric tube. CT pulmonary angiogram showed bilateral lower zone collapse and complete collapse of the left upper lobe with widespread ground-glass consolidation throughout the remaining aerated lung with an element of congestive failure. Despite pericardial drainage, she later developed type 2 respiratory failure and despite intubation and ventilation required transfer for surgical tracheostomy and long wean from ventilation. She was discharged on oral levothyroxine and nocturnal CPAP.

 

 

 

 

 

Discussion: Pericardial effusion is described in literature as a complication of myxoedema. These usually are exudative with high cholesterol content, but can occasionally be transudative

Respiratory failure is well recognised in myxoedema coma with reduced ventilatory response to carbon dioxide, decreased diffusion capacity, respiratory muscle weakness and decreased breathing capacity. Abnormalities suggestive of fibrotic lung disease have been described. Ventilatory response usually improves after treatment. In our patient, this did not happen and it took over two months to wean her off. Ground glass consolidation and hypoxia requiring prolonged ventilation and tracheostomy is very rare.

 

 

References

 

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