Lesson of the Week: Thyrotoxicosis in a patient with multiple trauma: value of “AMPLE” history takingBMJ 1996; 313 doi: https://doi.org/10.1136/bmj.313.7063.997 (Published 19 October 1996) Cite this as: BMJ 1996;313:997
- Jo Fitz-Henry, registrar in anaesthesiaa,
- Bernard Riley, consultant in anaesthesia and intensive carea
- Accepted 18 July 1996
In the highly charged atmosphere of resuscitating a critically injured patient the more mundane tasks such as taking a complete medical history may often be overlooked. We report a diagnostic conundrum which occurred because of this oversight.
A complete medical history should be taken from all patients with trauma using information from the patient, family and friends, and witnesses
A 26 year old tall, slim, white man was admitted to the accident and emergency department because of trauma to the left side of his body sustained in a motorcycle accident. Initial assessment identified an intra-abdominal haemorrhage and fractured left femur. He had a Glasgow coma scale score of 15 and no evidence of any head or neck injury. A history from the patient showed that he had been fit and well and was not receiving any drug treatment. He was taken to the operating theatre for an urgent laparotomy, splenectomy, and orthopaedic fixation of the fractured femur. He had persistent tachycardia in the operating theatre (heart rate 120–150 beats/minute) but maintained a good blood pressure and urine output throughout. During the four hour procedure he was given 5500 ml of intravenous fluids and 9 units of blood.
He was subsequently admitted to the intensive care unit for assisted ventilation and cardiovascular stabilisation. His heart rate was 150 beats/minute, intra-arterial blood pressure 180/60 mm Hg, and central venous pressure 3 mm Hg. He was considered to be fluid depleted, and vigorous fluid resuscitation was undertaken.
Six hours after surgery he had a temperature of 39.4°C and was sweating profusely, with a heart rate of 140 beats/minute, blood pressure of 110/40 mm Hg, and an obviously hyperdynamic circulation with a visible apex beat and a systolic flow murmur. There was no continuing blood loss and he was normovolaemic with a central venous pressure of 8 mm Hg, urine output of >100 ml/hour, and serum osmolarity of 297 mosmol/l. He was considered to be adequately sedated by morphine and midazolam infusions, having a Ramsay sedation score of 3.1 As he had sustained an injury to the left side of the chest in the accident, echocardiography was performed and showed a mildly dilated left ventricle with normal function. An electrocardiogram showed only a sinus tachycardia; there was no arrhythmia throughout his stay in intensive care.
This condition persisted for the next three days. His temperature decreased with active cooling of his skin surface, but he had a rebound fever each time this was discontinued. Extubation was deferred because of his high metabolic rate, oxygen requirement, and persistent tachycardia. Repeat cultures of blood, urine, and tracheal aspirate showed no sign of infection, although he had a persistent leucocytosis.
We had considered his hyperdynamic circulation and fever to be caused by the systemic inflammatory response syndrome as the result of trauma.2 A continuously monitoring Swan-Ganz pulmonary artery catheter gave his cardiac output as its upper limit default reading of 20 l/minute (cardiac index 9.8 l/minute/m2, normal range 2.5-3.5 l/minute/m2) and a systemic vascular resistance index of 546 dyn.s.m2.cm−5 (normal range 1900–2400 dyn.s.m2.cm−5). A noradrenaline infusion was started, but this made little difference to his systemic vascular resistance index, even in doses of up to 3.2 μg/kg/minute. Haemophilus influenzae was isolated from broncheoalveolar lavage fluid; his gas exchange was normal with a fractional inspired oxygen concentration of 35%, and a chest x ray film looked normal.
By day 7 he was considered to be ready for extubation. At this time his temperature was 37.7°C and his cardiac parameters were: heart rate 110 beats/minute, blood pressure 120/50 mm Hg, cardiac index 8 l/minute/m2, and systemic vascular resistance index 700 dyn.s.m2.cm−5. He required reintubation after only 20 minutes, when his respiratory rate was 48 breaths/minute. The following day he underwent a percutaneous tracheostomy. Although he had a long slim neck with no obvious swelling, there was a definite sensation of transmitted pulsation from the thyroid gland and the procedure itself was unusually bloody.
We then considered the possibility of thyrotoxicosis as causing symptoms of the systemic inflammatory response syndrome. His parents gave a family history of thyroid disease, and his sister was hyperthyroid. On direct questioning his girlfriend revealed that he had recently consulted his general practitioner because of severe night sweats and a failure to gain weight despite having a voracious appetite. Thyroid function tests showed severe thyrotoxicosis: tri-iodothyronine concentration was 19.5 pmol/l (normal 3.3-7.5), thyroxine 42.4 pmol/l (normal 12–24), and thyroid stimulating hormone <0.1 mIU/l (normal 0.4-5.0).
After treatment with propranolol, carbimazole, and hydrocortisone his thyrotoxic symptoms slowly settled, and he was successfully weaned from the ventilator as his oxygen requirement diminished. During the weaning process he required haloperidol for acute agitation—this may have been another manifestation of his thyrotoxic state.
In retrospect, the natural course of a thyrotoxic crisis had unfolded in a textbook manner in the pages of our notes. The commoner differential diagnoses for persistent tachycardia, fever, leucocytosis, and high cardiac output and low systemic vascular resistance in this patient after trauma were infection and the systemic inflammatory response syndrome. Intercurrent infection seemed unlikely in the presence of repeatedly negative results in cultures. The isolation of H influenzae from bronchoalveolar lavage fluid without clinical or radiological signs of chest infection suggested that this was a commensal organism. The liberation of inflammatory cytokines by direct tissue trauma is a potent trigger of the systemic inflammatory response syndrome, which produces signs identical with that of classic sepsis2 and thyroid storm.
The usual response to critical illness is a hypothyroid state.3 4 Studies have shown that diminished thyroid stimulating hormone activity precedes low concentrations of tri-iodothyronine and thyroxine. This hypothyroid state may be physiologically protective against excessive catabolism.
Direct trauma to the thyroid area (such as may be caused by the chin strap of a motorcycle helmet) has been documented as causing a traumatic thyroiditis, but is not known to cause an acute hyperthyroid state.5 From the history the family gave, the patient had obviously been thyrotoxic for some time before his accident.
This patient was fully alert and oriented on his admission to hospital and had histories taken by both the staff in the accident and emergency department and the emergency anaesthetic team, both of which failed to elicit his history of thyrotoxic symptoms. Though his family were interviewed by medical staff on many occasions in the first week, they were not questioned further about his medical history until the possibility of thyrotoxicosis was raised.
This case illustrates the need to obtain a full and accurate history. The Advanced Trauma Life Support Manual gives the mnemonic AMPLE for the essential information to be elicited from a trauma patient's history—that is Allergies, Medications, Past medical history, Last meal, Events or description of the injury.6 This information should be gained from the patient, their family and friends, and witnesses to the incident in all cases.
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