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Clinical
Details
A 78 year old lady presented with at least a
weeks history of abdominal pain and vomiting. She was mildly confused
and may have been unwell for longer. She lived alone and was on no
medication. General health was good and there was no history of cardiac,
renal or chest disease. Free gas under the diaphragm was visible on an
xray. She was thin and frail and was only mildly distressed. ECG showed
sinus rhythm. Amylase level was low. Clinical assessment was perforated
viscus with dehydration.
Initial blood results at 1000hrs in the Emergency
Department:
 |
Na+
137 mmol/l |
 |
K+
2.2 mmol/l |
 |
Cl-
91 mmol/l |
 |
HCO3-
38 mmol/l |
 |
urea 9.8 mmol/l
|
 |
creatinine 0.07 mmol/l
|
 |
albumin 21 g/l.
|
 |
[Hb] 91 g/l
|
Resuscitation with normal saline with potassium was
commenced. At operation, a dense pelvic abscess due to a perforated
pelvic appendicitis was found.
|
Serial
Blood Gas Results |
|
Number: |
1 |
2 |
3 |
|
Date: |
29th |
29th |
30th |
|
Time: |
1200hrs |
1730hrs |
0600rs |
|
Place: |
Emerg
Dept |
Operating
Theatre |
ICU |
|
FIO2 |
21% |
100% |
30% |
|
pH |
7.52 |
7.43 |
7.32 |
|
pCO2 |
44.6 |
42 |
45 |
|
[HCO3] |
35.8 |
27 |
22 |
|
pO2 |
59 |
94 |
81 |
|
Na+ |
137 |
141 |
|
|
K+ |
2.6 |
5.4 |
3.6 |
Assessment
The history and initial blood results strongly
suggest an acute metabolic alkalosis (elevated HCO3)
due to vomiting (loss of acid gastric contents) with typical findings of
hypochloraemia and hypokalaemia. The hypochloraemia prevents the kidneys
from excreting bicarbonate and maintains the alkalosis. The hypokalaemia
is potentially life threatening but significant muscle weakness was not
a complaint and there were no ECG abnormalities. The urea and creatinine
were not elevated despite significant dehydration. The patient was
maintaining some fluid intake.
Analysis of the initial blood gases collected after
resuscitation was underway confirm the metabolic alkalosis (ie
significant alkalaemia with elevated HCO 3).
Is the respiratory compensation appropriate? The
expected pCO 2 by rule 6 is
about 45mmHg [ie (0.7 x 36) + 20 ]. Respiratory compensation can be
variable in metabolic alkalosis but is almost exactly at the expected
level in this case. There is no respiratory acid-base disorder present.
The intraoperative gases later in the day are
interesting. Hyperventilation has been avoided as this can lead to an
acute respiratory alkalosis and cardiovascular deterioration. This is
not particularly important in this case though as the metabolic
alkalosis has been significantly corrected by this time. Blood gases in
ICU the next morning show complete resolution of the alkalosis and a
slight respiratory acidosis due to hypoventilation.
Other points:
The low albumin indicates chronic
poor nutrition. A low albumin level is also a cause of metabolic
alkalosis (see section 10.6) and this is relevant in this case. The
albumin level fell further with fluid loading.
Initial [Hb] fell with fluid
loading and the patient was transfused. The patient had a
significant anaemia and the haemoconcentration partly disguished its
severity.
A lactate level was not measured
in this patient. Hypovolaemia and poor perfusion especially if
associated with sepsis can cause lactic acidosis and a lactate level
will indicate the presence of a mixed metabolic disorder.
(Case 226042-98)
Firstly, initial clinical assessment (on the first gas results):
TO BE COMPLETED
Secondly, the
acid-base diagnosis:
1. pH:
2. Pattern:
3. Clues:
4. Compensation:
5. Formulation:
6. Confirmation:
Finally, the
Clinical Diagnosis:
Comment
Last
updated Sunday, 27 November 2005 06:19 PM
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