History: A 56 year old woman was admitted urgently to hospital with an acute abdomen. She had been unwell for three days, initially with vomiting then generalised abdominal pain and malaise. The pain was initially sharp and on the right side. She complained of not being able to breath properly. There was no significant past medical history.
She had smoked thirty cigarettes a day for many years. Her exercise tolerance was normally quite good. There was no history or clinical suspicion of ingestions of toxins. She was not on any routine medication.
Examination: She was alert and orientated but distressed. On arrival, BP was unrecordable & pulse rate 130/min. After IV fluid loading, BP 80 systolic (by oscillometry technique), pulse rate 110/min and regular. Pulse oximetry showed saturation of 86% on room air and 97% on high flow oxygen delivered via face mask. She was tachypnoeic with bilateral air entry. Peripheral pulses were weak and only intermittently palpable. Her abdomen was hard and distended.
Investigations: Initial pathology: Na+ 126, K+ 4.3, Cl- 83, HCO3- 14, Ca 2.52, Mg++ 1.06, glucose 4.8, urea 20.4, creatinine 0.31 (all in mmol/l); and [Hb] 191 g/l, white cell count 16,400. There was no gas under the diaphragm on a semi-erect chest film.
Arterial Blood Gases
pCO2 39 mmHg
pO2 277 mmHg
HCO3 14.9 mmol/l
In view of the patient's deteriorating condition, fluid resuscitation with crystalloids was commenced and she was transferred urgently to the operating theatre suite. Prior to induction of anaesthesia, she had received 2 liters of Normal saline and 2 liters of a modified gelatin colloid ('Haemaccel') for resuscitation. This brought her blood pressure up to 100 systolic and re-established some urine output but may have resulted in increased respiratory difficulty.
This assessment uses the structured approach outlined in section 9.1 and subsequent sections.
The patient has generalised peritonitis and was shocked. Initial clinical diagnosis was a ruptured viscus, possibly related to diverticular disease or an acute appendicitis, with gram negative sepsis.
An acid-base diagnosis of lactic acidosis was considered highly likely due to poor peripheral perfusion and sepsis. A metabolic alkalosis could be caused by the vomiting if it had continued and if such a mixed metabolic disorder was present, the bicarbonate level may not be very abnormal. The high haemoglobin level on presentation indicates significant haemoconcentration due to loss of fluid into the bowel (and absence of oral replacement fluid).
1. pH: The acidaemia indicates an underlying acidosis.
2. Pattern: The low bicarbonate and normal pCO2 suggests a mixed acid-base disorder: a metabolic acidosis with a respiratory acidosis. Alternatively, this pattern may be found if insufficient time had elapsed for respiratory compensation to have developed with an acute metabolic acidosis.
3. Clues: The anion gap is significantly elevated at 29mmol/l. Such a high level always indicates the presence of a high anion gap metabolic acidosis. A diabetic ketoacidosis is very unlikely as she is not a diabetic and the glucose is normal. The azotaemia is most likely pre-renal in origin but has reached the level where the renal failure may start to contribute to the metabolic acidosis. The hypochloraemia suggests a component of metabolic alkalosis due to vomiting.
4. Compensation: The expected pCO2 for an established metabolic acidosis is calculated from rule 5. In this case, the expected pCO2 is [(1.5 x 15) + 8] = 30.5mmHg. The actual value is higher than this indicating a co-existent respiratory acidosis. The history indicates that sufficient time has elapsed for respiratory compensation to have reached maximal.
5. Formulation: The high anion gap acidosis is probably a lactic acidosis. The hypochloraemia is noted and may indicated the presence of a component of metabolic alkalosis but this would be impossible to distinguish at this stage. The patient has an acute respiratory acidosis related to difficulty with ventilation due to the acute painful abdominal condition. There was no past history of respiratory disease.
6. Confirmation: A lactate level would confirm the diagnosis.
The lactic acidosis was due to the shock and the sepsis. The respiratory acidosis was acute and due to the rigid abdomen & the abdominal pain which made it difficult ('diaphragmatic splinting') for the patient to hyperventilate and compensate for the acute metabolic acidosis. This resulted in the sensation of dyspnoea.
The patient became centrally cyanosed prior to induction and despite administration of 100% oxygen via a close fitting mask and Anaesthetic circuit. This indicated the presence of a large shunt fraction.
She stopped responding to verbal communication even though her eyes were open. She was intubated after a rapid sequence induction. At laparotomy, liters of dark brown faecal material under pressure was removed from her peritoneal cavity. About 2500 mls was collected in sucker bottles and the drapes were flooded. A nasogastric tube was passed and 800 mls of similar fluid was drained from the stomach. A large perforation of a duodenal ulcer was found. Following the release of the abdominal tamponade the patient became pink centrally and was very much easier to ventilate.
The operation was completed at 1530 hours and she was transferred ventilated to the Intensive Care Unit. Over the next few hours she woke up and weaning from ventilation started as the patient commenced spontaneous respirations. Sedation was provided via a continuous infusion of a morphine-midazolam mixture. The following gases were collected at 1820 hours.
Arterial Blood Gases on 50% oxygen by endotracheal tube
pCO2 54 mmHg
pO2 104 mmHg
HCO3 21 mmol/l
|Other Pathology from Blood gas machine|
Na+ 136 mmol/l K+ 4.1 mmol/l Glucose 3.9 mmol/l Lactate 0.7 mmol/l
You should be able to answer the following questions:
Question 1: What is the acid-base diagnosis now?
Question 2: Why has this happened?