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Onco-emergencies

63

 

Atul Kulkarni and Vandana Agarwal

 

A 58-year-old male patient with metastatic renal cell carcinoma presented with lethargy, confusion, anorexia, nausea, and constipation. He was polyuric and polydipsic over the past few days.

63.1Hypercalcemia

Oncological emergencies such as hypercalcemia, tumor lysis syndrome, superior vena cava syndrome, and spinal cord compression are occasionally seen as an intercurrent problem or presenting manifestation in certain cancers.

Step 1: Resuscitate

Hydration is of utmost importance in these patients, and intravenous saline should be given rapidly once hypercalcemia is confirmed (refer to Chap. 78).

Step 2: Send investigations

Measure ionized serum calcium (arterial or venous).

If total serum calcium is measured, correct for the albumin level. Corrected calcium = measured total calcium + [0.8 × (4.0−albumin)].

Also, check serum creatinine, electrolytes, and alkaline phosphatase.

A low serum chloride level (<100 mEq/L) suggests hypercalcemia of malignancy.

ECG abnormalities reflect altered transmembrane potentials, affecting conduction such as QT interval shortening (common) and QRS interval lengthening (high levels). T waves may flatten or invert, and a variable degree of heart block may develop.

A. Kulkarni, M.D. (*) • V. Agarwal, M.D., F.R.C.A.

Department of Anaesthesia, Critical Care and Pain, Tata Memorial Hospital, Mumbai, India

e-mail: kaivalyaak@yahoo.co.in

R. Chawla and S. Todi (eds.), ICU Protocols: A stepwise approach,

499

DOI 10.1007/978-81-322-0535-7_63, © Springer India 2012

 

500

A. Kulkarni and V. Agarwal

 

 

63.2ECG Changes in Hypercalcemia

I

 

aVR

 

V1

 

V4

 

II

 

aVL

 

V2

 

V5

 

III

 

aVF

 

V3

 

V6

 

II

 

 

 

 

 

 

 

Device

Speed

25 mm / sec

L1 ab

10 aa / aV

Chest

10 aa / aV 40-0.5-4.0 W1 V

1w0701

The above ECG shows a short QT interval with hardly any ST segment, characteristic of hypercalcemia. In this tracing, the QRS complexes are wide, indicative of an intraventricular conduction defect. No P waves are evident, and this is most likely a junctional escape rhythm.

Step 3: Infuse fluid

Severe hypercalcemia is usually associated with marked hypovolemia.

Give 500–1,000 mL of normal saline in the first hour and continue at a lower rate until volume repletion is achieved and urine output is established.

In patients with impaired cardiorespiratory and renal function, aggressive fluid resuscitation should be done with close hemodynamic monitoring.

Step 4: Start diuretics after fluid repletion

Consider loop diuretics only when euvolemia is achieved, as hypovolemia causes renal hypoperfusion hampering calcium excretion.

Diuretics are specifically useful if features of hypervolemia, secondary to aggressive fluid resuscitation, develop.

63 Onco-emergencies

501

 

 

Table 63.1 Treatment for hypercalcemia

 

Intervention

Dosage

Comment

Normal saline

250–500 mL/h until euvolemic, thereafter

Caution in patients with

 

100–150 mL/h IV, may require 3–4 L

congestive heart failure

 

Keep urine output 100–150 mL/h

 

Furosemide

20–40 mg IV

After volume correction

Bisphosphonates

Pamidronate: 60–90 mg IV over 2–24 hours

Caution in renal impairment

 

Zoledronic acid: 4 mg IV over 15 min

 

Glucocorticoids

Prednisolone: 60 mg/day PO

Hyperglycemia,

 

Hydrocortisone: 100 mg IV every 6 h

immunosuppression

Calcitonin

4–8 IU/kg SC or IM every 12 h

Rapid onset but short lived

Step 5: Start specific therapy

Bisphosphonates block osteoclastic bone resorption.

Use zoledronic acid with caution in patients with renal impairment, and adjust the dose according to creatinine clearance (Table 63.1).

Subcutaneous or intramuscular calcitonin lowers calcium levels quickly, but the effect is short lived.

In some patients with lymphomas, particularly Hodgkin’s disease, hypercalce-

mia is caused by elevated levels of vitamin D (1,25(OH)2D); glucocorticoids are particularly effective.

Step 6: Decrease intake

Eliminate dietary sources of calcium.

Discontinue medications such as thiazide diuretics (increase the reabsorption of calcium) and vitamin D that increase the calcium level.

Step 7: Consider dialysis

Dialysis should be considered for patients with renal failure and/or congestive heart failure when aggressive hydration and bisphosphonates cannot be used safely.

Step 8: Treat the cause

Treat the malignancy with chemotherapy and radiation to control the hypercalcemia if possible.

Step 9: Evaluate prognosis

In patients with advanced malignancy, hypercalcemia may commonly occur.

In such circumstances, it may be appropriate, ethical, and humane to institute only comfort measures if no effective treatment for malignancy exists (Fig. 63.1).

502

A. Kulkarni and V. Agarwal

 

 

High index of suspicion

Measure serum calcium

Mild hypercalcemia 11 to 12 mg/dL

Asymptomatic

Hydration with saline Eliminate dietary sources of calcium and thiazide diuretics

Moderate hypercalcemia

Severe hypercalcemia

12 to 18 mg/dL

> 18 mg/dL

 

Symptomatic

Hydration with saline

 

 

Loop diuretics

 

Calcitonin

 

Bisphosphonates

 

Steriods if tumour responsive

 

Hemodialysis

Hydration with saline

Eliminate dietary sources of

calcium and thiazide diuretics

Loop diuretics when

 

euvolaemic

 

Bisphosphonate

 

Eliminate dietary

 

sources of calcium

Measure serum calcium and

and thiazide diuretics

other electrolytes following

 

 

treatment particularly serum

 

potassium at least twice a day till

 

calcium levels start decreasing

Fig. 63.1 Management of hypercalcemia

Tumor Lysis Syndrome

A 26-year-old patient with Burkitt’s lymphoma recently started on chemotherapy presented with anorexia, lethargy, disorientation, vomiting, muscle cramps, tachypnea, and decreased urine output.

Step 1: Resuscitate

These patients are usually dehydrated and will benefit with intravenous fluids (refer to Chap. 78).

Step 2: Make a diagnosis

Investigations may show hyperuricemia, hyperkalemia, hyperphosphatemia, hypocalcemia, uremia, and raised lactate dehydrogenase levels.

63 Onco-emergencies

503

 

 

Obtain electrocardiogram to rule out serious arrhythmias and conduction abnormalities.

Tumor lysis is associated with malignancies like acute lymphoblastic leukemia or Burkitt’s lymphoma with high tumor burden and responds rapidly to chemotherapy.

It usually follows chemotherapy, but may occur after radiation, corticosteroid therapy, or chemoembolization and rarely spontaneously.

Check urine output and renal function.

Step 3: Start hydration

A high infusion rate of fluids is appropriate.

Patients with high risk of tumor lysis syndrome should have aggressive volume replacement as a preventive measure prior to chemotherapy.

Infuse isotonic fluid at a rate of 200–300 mL/h.

Volume should be adapted for the patient’s age, cardiac function, and urine output.

Increasing the urinary flow rate is the most effective strategy for preventing urate-induced obstructive uropathy.

Urine output should be maintained within a range of 80–100 mL/m2/h (4–6 mL/ kg/h if <10 kg).

Urine-specific gravity should be maintained at £1.010.

Step 4: Use diuretics cautiously

Maintain adequate urine output.

It is contraindicated if hypovolemia or obstructive uropathy exists.

Step 5: Alkalinization of the urine

This was recommended earlier but is controversial as it can lead to the formation of urinary xanthine crystals.

This may cause obstruction of renal tubules if allopurinol is used concurrently.

It is not recommended with recombinant urate oxidase (rasburicase).

Step 6: Start allopurinol

Purine catabolism results in the production of hypoxanthine and xanthine, which are metabolized to uric acid via the enzymatic action of xanthine oxidase.

This pathway can be blocked by the use of allopurinol, a hypoxanthine analog that competitively inhibits xanthine oxidase.

Start allopurinol PO at 600 mg/day if uric acid is less than 8 mg/dL.

Allopurinol should be started prior to chemotherapy.

After about 2–3 days, allopurinol therapy results in increased excretion of both hypoxanthine, which is more soluble than uric acid, and xanthine, which is less soluble than uric acid.

A marked increase in xanthine excretion can occur when allopurinol is given for prevention of tumor lysis syndrome and may lead to acute renal failure or xanthine stones.

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