Collapse in a Patient Undergoing Chemotherapy Case Study in Pathology

In this post, we are going to discuss the disease Collapse in a Patient Undergoing Chemotherapy.

History:

A 30-year-old man undergoing his second cycle of Adriamycin, bleomycin, vinblastine, dacarbazine (ABVD) chemotherapy for bulky stage II Hodgkin’s lymphoma is brought into hospital by his wife after collapsing at home. His wife says that the patient has been vomiting several times over the past 24 hours and has been complaining of increased fatigue. Though drowsy, he says that he has been experiencing numbness in his hands over the past couple of hours as well.

Examination:

Physical examination reveals a sickly-looking man with cool peripheries. His vital signs show T 36.2°C, BP 95/60, HR 100 and fair, RR 24, and air O2 saturation 95%. An ECG shows peak T waves and QRS prolongation (0.14 ms). Glucose from a finger prick is 5.6 mM and capillary refill time is 3 s. GCS is 14/15 (E4, V4, M6). Given his clinical status, the patient is catheterized and urine output is 10 mL in the first thirty minutes, improving to 25 mL in the next thirty minutes after fluid resuscitation.

Haemoglobin;11.9
White cells; 5.6
Platelets; 180
Sodium; 133
Potassium;6.3
Urea; 15.9
Creatinine; 156
Bilirubin;10
Alanine aminotransferase;25
Aspartate aminotransferase; 30
Alkaline phosphatase; 110
Corrected calcium;1.65
Phosphate; 1.8
International normalized ratio; 1.1

 Requirement:

1. Renal function is grossly deranged in this patient. What are the possible causes of
this and how may they be differentiated?
2. Given the clinical picture and test results, suggest an underlying aetiology for this
patient’s presentation.
3. Discuss the pathophysiology of the likely underlying diagnosis.
4. What are the main aspects in managing this patient in the acute setting?

 Solution:

This patient has acute renal failure, which can be defined as rapid loss of renal function with retention of urea, creatinine, and other metabolic products, and is often characterized by oliguria. His urea and creatinine levels are around 1.5 times the upper limit of normal, while his urine output (before fluid resuscitation) of 20 mL/hr is significantly lower than expected in an adult male. Classically, the causes of acute renal failure are classified as:

• Prerenal, arising from hypovolemia leading to inadequate renal blood flow (hemorrhage, sepsis, heart failure, diarrhea, and use of diuretics)

• Intrinsic renal disease, which can affect the glomeruli (eg, various glomerulonephritis), the tubules, and the interstitium (eg, drugs such as NSAIDs and aminoglycosides, contrast media, and intrarenal obstruction from kidney stones or cast nephropathy in multiple myeloma), or the blood vessels (eg, vasculitis, hypertension, diabetes)

• Postrenal obstruction, leading to renal failure when both outflow tracts are obstructed or when one is obstructed in patients with only one kidney (eg, obstruction of the bladder outflow, ureteral stones, intratubular crystal nephropathy, and urothelial neoplasms) Urine measurement.

The composition and use of urea ratios are rich: creatinine can help differentiate between the above when the history is not particularly suggestive, as shown below.

Measurement Prerenal Renal Postrenal

Urine osmolality (mOsm/kg) >500 20 >40

Fractional Na excretion (%) 2 >4 Serum

Ur:Cr >100:1

Given the patient’s hypovolemic state, which predisposes the patient to developing insufficiency kidney disease, the priority for immediate management is fluid resuscitation. Hydration also helps minimize acidosis and increases urine pH, which reduces the risk of urate crystallization. Hyperkalemia requires intervention with calcium gluconate, insulin, and dextrose, since ECG changes present with increased risk of arrhythmia.

The other metabolic abnormality that requires urgent intervention is hyperuricemia. Rasburicase, which converts uric acid to the inactive, soluble metabolite allantoin, is preferred over xanthine oxidase inhibitors such as allopurinol, since rasburicase also breaks down existing uric acid, while allopurinol only prevents its formation. Patients with clinical TLS often also require treatment in an ICU setting, given the need for cardiac monitoring and supportive treatment of renal failure by haemofiltration.

 

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