Case History 14 : A man with an out-of-hospital cardiac arrest
Clinical
Details
A 54 year old man was
admitted following an out-of-hospital cardiorespiratory arrest.
His wife said he had complained of indigestion on and off for the past 2 months. He had attended his local doctor the previous day with upper abdominal pain and a cough. He was commenced on an antacid and erythromycin. That night the pain had become much more severe. The After-hours Locum Service was called and he was given IM morphine. The pain was severe again the next day. He collapsed at home at about 1200 hours.
The ambulance arrived about 5 minutes later. The ambulance officers diagnosed a cardiorespiratory arrest because the patient was comatose (GCS 3/15), pulseless and apnoeic. Cardiopulmonary resuscitation was commenced. After 5 minutes, the patient had a palpable pulse and was breathing. On arrival at hospital he was awake and able to give a history. He complained of severe abdominal pain and was guarded in the upper abdomen. Blood pressure of 80 systolic increased with fluid loading. The only past history was of hypertension but he was on no medications. A pneumoperitoneum was seen on a semi-erect chest xray. At urgent laparotomy, a perforated duodenal ulcer and gross peritoneal soiling was found. Fifty mls of 8.4% sodium bicarbonate was given intraoperatively at 1345hrs following arterial gases at 1330hrs. Postoperatively, he was transferred ventilated to the Intensive Care Unit. Serial results are listed in the table.
|
Serial Biochemistry & Arterial Gases |
||||||
|
Time: |
1245 |
1330 |
1500 |
1715 |
0625 |
0720 hrs |
|
Na+ |
143 |
|
141 |
|
|
141 |
|
K+ |
5.6 |
|
4.5 |
|
|
5.3 |
|
Cl- |
106 |
|
108 |
|
|
115 |
|
HCO3- |
7.1 |
|
10.7 |
|
|
22 |
|
Glucose |
3.6 |
|
8.1 |
|
|
5.4 |
|
Urea |
11.4 |
|
11.0 |
|
|
13.5 |
|
Creatinine |
0.30 |
|
0.22 |
|
|
0.16 |
|
Lactate |
9.3 |
|
|
|
|
|
|
Anion gap |
30 |
|
22 |
|
|
4 |
|
pH |
6.89 |
7.14 |
|
7.28 |
7.38 |
|
|
pCO2 |
32 |
25 |
|
32 |
32 |
|
|
[HCO3] |
5.6 |
8.3 |
|
15.2 |
18.4 |
|
|
pO2 |
244 |
283 |
|
180 |
144 |
|
Assessment
Firstly, initial clinical assessment (on the first gas results):
Secondly, the
acid-base diagnosis: (to be completed)
1. pH:
2. Pattern:
3. Clues:
4. Compensation:
5. Formulation:
6. Confirmation:
Finally, the Clinical Diagnosis:
Diagnosis
A severe acidosis is evident on the initial gases. In
view of the history, the pCO2
less then 40mmHg and the large anion gap, this is clearly a severe
primary metabolic acidosis. A lactic acidosis due to poor perfusion and
related to sepsis is present. The lactate level measured over 3 hours
after arrival at hospital was very high (9.3 mmol/l). The renal
threshold for lactate is about 5 mmol/l so some lactate may be lost in
the urine once urine output is reestablished.
Pre-renal renal failure was present and this will probably have contributed to the metabolic acidosis. Acidosis (and hyperkalaemia) in chronic renal failure does not occur until the GFR is less than 20 mls/min (corresponding to a creatinine level of 0.30-0.35 mmol/l ). The creatinine level in acute renal failure will initially tend to underestimate the actual level of renal impairment as the rise in creatinine takes time to occur.
Note that the decrement in [HCO3] is about 18 mmol/l. This matches the rise in the anion gap (ie from 12 to 30) but is more than the rise in the lactate level. This strongly suggests the presence of acid anions other than lactate. In pure lactic acidosis, the anion gap increment is usually greater than the bicarbonate decrement because of substantial intracellular buffering.
It should be noted that the pCO2 is inappropriately high for the severity of the metabolic acidosis in this patient. The predicted pCO2 is about 16 mmHg. It sometimes takes about an an hour or two for much compensatory hyperventilation to occur but 12 or more hours are required for full respiratory compensation. Upper abdominal guarding due to pain has probably limited the increase in ventilation and there may be a component of respiratory acidosis in this case. The initial pH is critically low reflecting the severity of the acidosis and the lack of ventilatory compensation.
The management consisted of assessment, restoration of the circulation with volume loading, surgery and postop ventilatory support and monitoring in the Intensive Care Unit. It is difficult to provide adequate pain relief following major upper abdominal surgery in an elderly patient without depressing ventilation. A rise in the pCO2 would have caused worsening of the intracellular acidosis and negative inotropic effects with circulatory instability.
The mortality rate associated with a lactate level as found in this patient is about 90%. This patient survived and was discharged from hospital.