Coroner's Court of Queensland - Investigation into the death of Mr B Coroner's Court of Queensland - Investigation into the death of Mr B

Coroner's Court of Queensland - Investigation into the death of Mr B

9 November 2016 | Health Sector

Aboriginal man dies from complications of an undiagnosed subdural haematoma when his symptoms were incorrectly attributed to alcohol withdrawal.

Date of findings: 15 September 2016
Coroner: Ainslie Kirkegaard
Inquest Place: Brisbane
Date of death: 31 March 2015

Issues for Consideration

  • Concerns there may have been an earlier opportunity for diagnosis.

Factual Summary

Mr B, a 41 Aboriginal man died at a Regional Base Hospital (RBH) on 31 March 2015 from complications of an undiagnosed subdural haematoma. He had a history of alcohol abuse.

He presented to the Rural Hospital (the hospital) four times between 24 February and 29 March complaining of headache. On his later presentations, many of his additional symptoms (such as unsteadiness and significant tremor) were attributed to alcohol withdrawal.

Evidence

Hospital & Health Service (HHS) clinical review outcomes

  • In the absence of trauma or neurological symptoms, the assessment and management of Mr B on 24 February 2015 was probably reasonable.
  • There was a failure to recognise the significance of Mr B’s ongoing headache. On 28 March 2015 Mr B’s score was 9/10 but this was not reflected in the triage score.
  • Assessment on 29 March 2015 attributing his presentation to alcohol withdrawal was probably reasonable given the documented intake on this and previous episodes. Mr B reported that he had not had alcohol for four days and it would have been reasonable to expect Central Nervous System (CNS) symptoms.
  • However, the history of tremors prior to admission may have confounded the clinical picture (tremors were disregarded for the Alcohol Withdrawal Scale (AWS)) and meant that a higher dose of diazepam was administered (for treatment of alcohol withdrawal).
  • The high doses of diazepam confounded the interpretation of Mr B’s change in level of consciousness which, in hindsight, most likely indicated pathophysiological changes associated with subdural haemorrhage.
  • There was a delay of 1 hour in notifying a doctor when Mr B was assessed to be comatose and to have fixed and dilated pupils. While this delay probably did not change the outcome, there was still a failure to recognise his clinical deterioration.
  • There were no specific neurological observations apart from those in the AWS record.

Independent clinical review

  • It was apparent that Mr B’s symptoms on presentation were viewed more in the context of his history of excessive alcohol intake rather than investigating other possible explanation for headache. Given, Mr B’s history and his signs and symptoms (particularly the later presentations when a tremor was present) this was not unreasonable.
  • Management of acute alcohol withdrawal required the use of diazepam which causes CNS depression and can not only mask signs of deterioration in a head injury, but also simulate them.
  • In the absence of CT scanning equipment, it is unlikely that Mr B might have been diagnosed prior to 28 March 2015 and, even if identified then, there was no guarantee that the subdural haemorrhage would have been amenable to curative treatment bearing in mind that Mr B would have required transport to a larger hospital to manage his condition neurosurgically.

Conclusions

  • Mr B died from complications of undiagnosed subdural haematoma.
  • Mr B’s presentations over the period from 24 February – 29 March 2015 represented a missed opportunity to have explored the possibility of intracranial haemorrhage, however, this was not unreasonable in the context of Mr B’s history and presenting signs and symptoms, particularly when the tremor was present.
  • There were opportunities during Mr B’s admission over 29-30 March for hospital staff to have recognized and responded to his clinical deterioration sooner. However, even if that had occurred it was accepted that it is unlikely medical intervention at that point in time would have changed the outcome.
  • The new Queensland Adult Deterioration Detection System (Q-ADDS) (version 6) was not in use at the time (and had subsequently been implemented) and would have trigged a medical review at 8:00pm on 29 March 2015.

Recommendations

Use and compliance with the new Q-ADDS has been the subject of recent coronial inquests. It was noted that the HHS had now implemented that new Q-ADDS (which was not in place at the time).

Chronology of Events

24.02.2015
10:55AM

Mr B presented to the Rural Hospital emergency centre complaining of onset of pain over the right mandible and spreading to the right eye with headache over 5-10mins which he rated as 9/10.

The attending doctor performed a neurologic examination which showed some mild increase in light touch sensation on the right.

Mr B was diagnosed with a cluster migraine and treated with high flow oxygen, paracetamol, ibuprofen and vitamin B.

11:45AM Mr B's pain score had dropped to 5/10
3:05PM Mr B was discharged
03.03.2015
8:00PM

Mr B presented to the hospital complaining of 2-3 days of generalized headache associated with neck pain and tension. His pain score was 4/10.

Mr B was treated with paracetamol and indomethacin suppository (a non-steroidal anti-inflammatory) which resulted in almost total resolution of his pain.

10:25PM Mr B discharged
28.03.2015
1:00PM

Mr B presented to the hospital complaining of severe headache (9/10). He reported having taken paracetamol before calling the ambulance.

On examination his pupils were equal in size and reacting to light, no photophobia. He had vomited twice the previous day in association with headache. He reported only having “a couple of beers” that day. The triage nurse also noted an underlying tremor.

Mr B was not examined by a doctor. The triage nurse spoke to a doctor on the phone who advised giving 1 litre of intravenous saline, 10mg maxolon for vomiting, intramuscular ketorolac (non-steroidal anti-inflammatory) and codeine phosphate.

4:15PM Intravenous therapy was completed.
4:20PM Mr B discharged.
29.03.2015
7:28PM Mr B presented to hospital complaining of ongoing headaches and vomiting
7:40PM

Pain score of 6/10 recorded. Mr B was noted to have unsteadiness, a significant tremor, headache and nausea which he attributed to alcohol withdrawal, noting that Mr B had not consumed alcohol for 4 days.

He was commenced on intravenous fluids, Nexium (proton pump inhibitor anti-ulcerant) and diazepam per Alcohol Withdrawal Scale (AWS) guidelines.

30.03.2015
4:00AM Mr B was noted to be restless and his headache pain rating was 6/10. He was given panadeine and diazepam per the AWS guidelines.
10:00AM Mr B reviewed by doctor. Headache described as a sharp band and he was noted as having “no neurology” and “CNS grossly intact”.
2:30PM

Mr B noted to be “drowsy ++” and incontinent of urine.

The nurse gave his diazepam per AWS guidelines. The nurse contacted the doctor and was advised to disregard the tremor when calculating the AWS score.

4:30PM Mr B’s pupils were 5mm in size and equal but not reacting to light
4:40PM Mr B incontinent and asleep/snoring
5:35PM Mr B found unresponsive. He was breathing and vomited before deteriorating rapidly. He went into cardiac arrest. He was resuscitated after approximately 4-5mins.
 

Mr B transferred to the Regional Base Hospital (RBH). He was intubated, mechanically ventilated and treated with broad spectrum antibiotics.

A CT showed a large right-sided acute on chronic subdural haematoma with evidence of midline shift and compression of the right lateral ventricle of the brain, compression of the left side of the brain and evidence of herniation.

Mr B was admitted to the intensive care unit. His condition was discussed by the neurosurgical team at the Tertiary Hospital and it was considered that he had an unsurvivable brain injury.

2:10AM Active treatment withdrawn, Mr B extubated and died half an hour later
Autopsy revealed hypoxic brain injury and acute on chronic subdural haematoma and bilateral severe aspiration pneumonia. There was evidence of past blood staining and older bleeding.
Robert Samut

Robert Samut

Principal