Monday, 26 February 2007

History and Physical Revisited: a neurological quandry

This case has been anonymised for patient confidentiality.

A male patient of advanced age who presented with a sudden history of collapse. The patient apparently did not lose consciousness and returned to his home. Following this, the patient's conscious level began to decrease, and his breathing became laboured and his family admitted him to hospital.

It was not clear exactly what was described when the patient's breathing became abnormal. For example, did respiratory rate increased or decrease? Did the patient develop asthma-like symptoms, was there any pulmonary oedema, cough, sputum, haemoptysis?

Also, there is no history about what happened before the collapse. Where was the patient? What was he doing? Was there a sudden onset of headache? Were there any other features? Was there seizure activity and if so, was it sustained?

With the paramedics attending his home, his GCS was described as 3/15 but on admission to hospital, the GCS had apparently increased to 14/15 and the patient was able to speak and follow commands during examination.

However, following this, his breathing became further laboured with there being identification of hypoxaemia on blood gas analysis and the patient was intubated and ventilated.

The patient had not apparently sustained any head injury but other details of history such as sudden onset headache / chest pain / neck stiff were not elicited.

The previous medical history was that of hypertension only for which he took medication, although on admission, it was not known what medication he was taking.

Vitals signs were slightly abnormal, with the patient being normotensive, afebrile but with a of pulse 100/min and regular.

From what was relayed to me, the CNS examination was relatively unremarkable and the only positive finding on the rest of the physical examination were bilateral crackles at both bases on chest exam.

The patient had had the usual tests including chest Xray and Chest CT which showed old changes which looked like fibrosis, but there was no obvious pneumonia.

CT head showed a very small area of fibrosis near the thalamus on the right side, but this looked old. There was no blood or space occupying lesion (SOL). The MRI scan showed no abnormality apart from some artifact over the left frontal area. The diffusion MRI was otherwise normal.
The vascular scan showed no obvious abnormality.

Bloods revealed a slightly raised BUN of 27 but a normal creatinine. White cell count was slightly raised and CRP was increased to 2.1. CK, CK-MB, Troponin T were all normal. All other usual bloods were normal.

ABG- revealed a normal pH but CO2 and HCO3 were decreased and the SpO2 was approx. 50mmHg consistent with a compensated respiratory alkalosis and hypoxaemia.

The team were concerned that a pneumonia may be causing the chest symptoms but were unable to ascertain the cause for the collapse and coma, especially as the examination and tests had been normal.

My Opinion.......

On hearing this rather brief history, the differentials that come to mind include:

  • Subarachnoid haemorrhage -- initial collapse from bleed and then as vascular constriction ensues, and intracranial pressure increases, the patient can become comatosed from ischaemia. Some SAH cannot be picked up on CT and only a Lumbar puncture performed, usually after 18 hours will pick up Xanthochromia.
  • Stroke: a sudden onset phenomenon with sudden loss of neurological function either from infarction or bleeding. When considering thrombotic stroke, one should remember that thrombo-emboli can originate from the heart chambers, the valves, myxoma, platelet rich emboli from the carotids and primary thrombosis from atherosclerotic plaques. Paradoxical embolus and stroke can occur from a patent foramen ovale giving a right to left shunt through the atria. Emboli can pass from right to left cardiac circulations and cause stroke! This however is very rare. Patients may regain some level of consciousness but this may deteriorate with cerebral oedema.
  • Sudden Cardiovascular Collapse: Loss of cardiac output for any reason such as a dysrhythmia, can lead to collapse and patients may suffer cerebral hypoxia and brain damage or head injury. With the latter, injuries to the temporal area can cause laceration of the middle meningeal artery and tense extradural bleeds and reduced consciousness.
  • Dissection: Dissection can lead to acute collapse from sudden loss of valvular competency and / or tamponade, and if there is a proximal dissection, it can occlude the arteries supplying the head and neck leading to stroke.
  • Pulmonary Embolism: Large PEs can cause sudden collapse and unconsciousness due to sudden cardiovascular compromise. PE can be chronic in nature and cause fibrotic change. Hypoxaemia from a massive PE can lead to hypoxaemia and reduced conscious level.
From the scans and data, there was neither an obvious large stroke nor an SAH. There was no evidence of a dissection or head injury either. The CT chest, which showed contrast imaging of the pulmonary vessels, did not reveal any PE.

Further results revealed a normal CSF examination with a slightly raised protein level only.

Urine results revealed no sugar but two plus of ketones (probably explained by fasting state)

Blood sugar approx 210. Could have this been an undiagnosed DKA with respiratory compensation??? I think unlikely in view of the absence of glucose in the urine.


Examination of the patient was difficult due sedation from propofol. However, at the end of the bed, the patient was making some unusual movements of adducting his shoulders and turning his wrists slightly inwards. He also had twitches which I thought might be sub-clinical seizure activity.

On examining him, his pupils were approx 4mm bilaterally and responded rapidly to light and were hence intact. Response to pressure on the nailbeds on both hands revealed Extension to Pain. Babinski responses were bilaterally positive as was Achille's Tendon Pinch which also causes plantar extension. Just to ensure that this was not just a withdrawal response, the patient was tested with a noxious stimulus, which in the case was a blunted pin. A normal response should be to plantar flex away from the pin tip when applied to the dorsal aspect of the toe. A positive response is dorsiflexion towards the pin tip. This patient showed bilateral Positive Signs confirming bilateral Upper Motor Neurone impairment.

Chest examination revealed bilateral crackles with them being of higher intensity of the right side.

Clinical Impression

Following this most revealing examination, it showed that the patient actually had developed severe neurological signs. With the signs being Bilateral this suggested that both cerebral hemispheres had probably become involved.

With the patient Extending to pain, this is a decerebrate condition. However, his pupillary responses were spared and when examined by a very astute neurologist, the Doll's Eyes reflex was also normal suggesting a normal midbrain.

Hence, a definite abnormality was identified which could now account for some of the features of the history.

The basic neurological examination helped reveal the problem that no scan could identify.

This underlines the importance of a good history (where possible from the patient / family /friend /bystander) and detailed physical examination.

Please remember that detailed physical examination should be able to reveal gross physical abnormalities. When performing a neurological examination on a conscious or unconscious patient, the Babinski Response can be of paramount importance. There are many other tests for finding upper motor neurone signs such as Hoffman's Sign in the fingers and many other in the feet which can be found in any good neurology textbook.

Don't forget to check for Clonus as more than three beats is signifcant og UMN signs.

Don't forget the Reflexes. It does not take long to do but can reveal the possible level of the problem and determine absent, decreased, normal or increased reflexes, which are all significant of either normal or abnormal neurological states.

Don't forget to do sensory testing in the conscious patient as this again can determine the level of a lesion.

This patient had a repeat scan but again this was normal.

After discussion with the neurologist, it was suggested that the clinical features and a normal set of scans with 24 hours of admission could be accounted for by:

  • Diffuse bilateral hypoxic-ischaemic damage of the cerebral hemispheres
  • Multiple embolic phenomena
Hence, the history of sudden collapse and waxing-waining consciousness might be accountable from a cardiovascular cause leading to cerebral ischaemia or multiple infarction.

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