Croydon, UK
EditorWe read with interest the case report on neurological outcome prediction in a cardiorespiratory arrest survivor by Goh and colleagues.1 We would like to report a similar incident which occurred in our hospital.
A 45-yr-old male collapsed suddenly in the street. The person who witnessed the collapse alerted the London Ambulance Services within 10 min. When the paramedics arrived 8 min later, there was no respiratory effort and no palpable pulse. The ECG monitor showed ventricular fibrillation. Sinus rhythm was restored after the first DC shock of 200 joules. The carotid pulse became palpable and the heart rate was 106 beats min1. Arterial pressure was 102/53 mm Hg. The patient started to breathe but remained unconscious with a Glasgow coma scale of 3. The cervical spine was stabilized with a hard collar. Tracheal intubation was attempted by the paramedics but failed. The airway was maintained with a Guedel airway and jaw thrust. The respiratory rate was 56 bpm. Oxygen 15 litres was administered via facemask with a reservoir bag. An oxygen saturation of 96% was achieved at the scene and the patient was transferred to our hospital.
On arrival in the accident and emergency department, the patient was making spontaneous respiratory effort and his oxygen saturation was 95%. Air entry was poor bilaterally with coarse basal crepitations. The heart rate was 90 beats min1 with an arterial pressure of 100/50 mm Hg. The Glasgow coma scale improved to 5/15. He was moving all four limbs to painful stimulation. The pupillary size was 3 mm bilaterally and sluggishly reactive to light. Following preoxygenation and rapid sequence induction, the trachea was intubated without any complications. Sedation was maintained with a propofol infusion. A bolus of atracurium was administered to facilitate intermittent positive pressure ventilation. A 12-lead ECG showed sinus rhythm with non-specific ST segment abnormality. An urgent CT scan of head did not show any abnormality. Cervical spine x-rays were normal. Chest x-ray revealed consolidation of the right middle and lower lobes secondary to aspiration. The patient was transferred to the intensive care unit (ITU) for further management.
During his stay in ITU, the patient's clinical condition was complicated by convulsions and sepsis. The first episode of convulsions occurred 7 h after the cardiac arrest. This initially responded to phenytoin 1.35 g and Diazemuls 10 mg. Phenytoin 300 mg was continued once daily. Further seizure activity required treatment with Diazemuls and sodium valproate. Sedation was maintained with infusions of propofol, midazolam and alfentanil. He remained stable cardiovascularly, initially requiring epinephrine 0.6 µg kg1 min1, which was later weaned and substituted by dobutamine 7.5 µg kg1 min1. An echocardiogram showed a normal size left ventricle with reasonable systolic function. The right ventricle was dilated with poor systolic function and the right atrium was mildly dilated. EEG revealed epileptic activity correlating with the clinical signs. The troponin T level on day 3 was 0.08 µg litre1. Pulmonary angiogram performed on day 7 showed no evidence of pulmonary embolism. Percutaneous tracheostomy was performed on day 10. Despite anticonvulsant therapy, the patient continued to have seizures and adopted a decorticate posture. In view of this, the poor prognosis was discussed with the family and a decision was made not to resuscitate in the event of cardiac arrest.
However, from day 11, the patient made a dramatic improvement in neurological function. He responded appropriately to conversation and began obeying commands. The decision not to resuscitate was therefore cancelled. The GCS gradually improved to 15/15. Respiratory support was weaned. By day 14, the patient was able to sit up in bed but could not maintain his balance. The seizure activity gradually decreased and he demonstrated full power in both arms and legs. Sensation in both limbs was normal and he had no contractures. On day 20, he was able to mobilize in the ITU using a Zimmer frame, but still continued to have difficulty in coordinating movements. The tracheostomy was sealed with occlusive dressing. He could eat a normal diet. He was then referred to the rehabilitation unit for further management. He made a complete physical and neurological recovery by day 29, including past and recent memory. He is due to be discharged home soon. He is booked for an elective coronary angiogram.
We believe that our patient suffered cerebral hypoxia during cardiorespiratory arrest possibly secondary to a coronary event. This may have caused a period of ventricular tachycardia and led to no cerebral perfusion for up to 18 min. He did not have any CPR during this period. Despite restoring cardiac output after the first DC shock of 200 joules, he remained unconscious. Duration of anoxia and postanoxic coma are considered prognostic indicators. Our patient adopted a decorticate posture and experienced generalized seizures. He had no history of epilepsy. In the ICU, the patient continued to have clinical and EEG evidence of epileptic activity, which was difficult to control. The patient also developed generalized myoclonic jerks. Similar to the case report by Goh and colleagues,1 our patient too, in spite of these poor prognostic features, made a good neurological recovery. It is possible that there was some on-going systemic perfusion during the collapse, which was followed by ventricular fibrillation.
Conventional clinical and EEG assessment of neurological recovery from cerebral hypoxia after cardiac arrest can be misleading. With the current paucity of ITU beds, it is difficult to determine time periods in resuscitation policies. Both Gohs patient and our own have shown that unexpected improvement can occur. Therefore the decision not for resuscitation needs to be reviewed in the light of unexpected neurological improvement.
R. Srikiran
G. Menon
Croydon, UK
References
1 Goh WC, Heath PD, Ellis SJ, Oakley PA. Neurological outcome prediction in a cardiorespiratory arrest survivor. Br J Anaesth 2002; 88: 71922