Abnormal Pharmacology and Nausea
Try out this pharmacology case and test your clinical knowledge. The answers are at the bottom.
A 32-year-old woman presents to A&E with vomiting and nausea. She tells you that she was recently diagnosed with a UTI from her GP and started on gentamicin.
High BMI (41)
POC Bladder US: 500 ml pre-void, 298 mls post-void
Good anal tone
Q1: Calculate her NEWS2 score. What is the significance of this result?
Some initial bloods are taken
|FBC||142||135 – 180 g/l|
|MCV||87||80 – 100|
|WCC||10.3||4 – 11 x 109/l|
|Plts||180||150 – 400 x 109/l|
|Urea||50.1||2 – 7 mmol/l|
|Creatinine||631||55 – 120 umol/l|
|Uric Acid||0.41||0.18 – 0.48 mmol/l|
|Na+||130||135 – 145 mmol/l|
|K+||5.8||3.5 – 5 mmol/l|
|ALP||89||30 – 100 umol/l|
|ALT||21||< 42 IU/L|
|PTH||5.1||1.6 – 6.9 pmol/l|
|Ca2+||2.4||2.1 – 2.6 mmol/l|
|Phosphate||0.9||0.8 – 1.4 mmol/l|
|AST||28||< 40 IU/L|
|GGT||50||< 60 IU/L|
|Bilirubin||3||< 21 umol/l|
|pH||7.28||7.35 – 7.45|
|HCO3||13||22 – 29 mmol/l|
|PaO2 (corrected for FiO2)||16.2||10 – 13.3 kPa|
|PaCO2||2.3||4.7 – 6 kPa|
|Lactate||0.9||0.5 – 1 mmol/l|
Q2: Comment on the bloods. What is the diagnosis?
Shortly after presenting to A&E she collapses and becomes unresponsive. A pulse is palpable. An ECG is performed which shows:
Q3: Comment on the ECG. What is the likely complication?
Q4: How would you manage this complication?
Reveal the Answers
Total: NEWS 8
A NEWS score of 8 indicates a ‘high’ level of risk and warrants anurgent/emergency assessment by senior clinicians. This patient is very unwell and ITU should also be informed.These patients are often automatically triaged by critical care outreach teams once their NEWS reaches 7.
The most striking abnormality is in her renal function. This is most likely an AKI as even though we do not have previous renal function results to compare with, the normal calcium and phosphate point to an acute deterioration in renal function (in CKD hypocalaemia often leads to an increase in PTH–secondary hyperparathyroidism which subsequently sequesters phosphate in the blood). Similarly, the lack of a normocytic anaemia secondary to a chronic reduction in the ability of the kidneys to produce EPO points to an acute kidney pathology.
Her Urea: Creatinine ratio is < 100 and as such implies an intrinsic renal cause of her deterioration, as opposed to a pre-renal cause e.g. dehydration/shock or renal artery stenosis. The most likely culprit here is an inappropriately high gentamicin dose by her GP, as the drug is dosed by a patient’s ideal body weight NOT their actual body weight due to gentamicin’s poor lipid solubility. Gentamicin is renally excreted and at toxic doses can lead to acute tubular necrosis and subsequent AKI.
The uraemia is driving her metabolic acidosis, with partial respiratory compensation (hyperventilation).
Her electrolyte disturbance is a common picture in AKIs, with sodium being haemodiluted due to the extra fluid retained and potassium being withheld within the bloodstream due to the acidosis.
This is in essence ventricular tachycardia with features of:
-Broad QRS > 120ms
However, the distinguishing feature of thetall, tented T-waves points to the underlying cause of this arrythmia–severe hyperkalaemia. This is likely secondary to her AKI combined with her ACE inhibitor, which further increases blood potassium levels.
An A-E approach should be adopted, and she will likely require intubation and ventilation. Hyperkalaemia is usually managed as follows:
-Calcium chloride (10ml of 10%)–This stabilizes the cardiac membrane and prevents further arrythmias
-Insulin/dextrose infusion (50 units actrapid in 50 mls 20% dextrose)–this drives the potassium into cells, reducing the serum K+ concentration
-In more severe cases, calcium chelators e.g. calcium resonium and haemofiltration can also be used
Image 1: https://litfl.com/wp-content/uploads/2018/08/ECG-Hyperkalemia-serum-potassium-9.3.jpg”>rID: 7529
University of Cambridge
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