Oncological

Emergencies

{ SUPERVISED BY: DR. WALEED KALEEM

A 70 years old male known case of •
lymphoma and under chemotherapy came
to emergency room in unconscious state,
the blood pressure was 90/60 mmHg,
irregular pulsation, ECG show atrial
fibrillation. After resuscitation the patient
admitted to intensive care unit.

By history: patient had fever, fatigue,

nausea and vomiting, muscle cramps,
tetany, hematuria flank pain and epistaxis
By physical examination:
patient was febrile , there was petechia all around
the body.

Investigation:

WBCs: 3000 /µL

Hemoglobin: 9 g/dL
Platelets: 20000 /µL
Calcium: 6 mg/dL
Potassium: 6 mmol/L
Uric acid: 10 mg/dL
?What is the possible diagnosis
 Oncological
emergencies

Hematologi Treatment-
Metabolic
c Structural
related

Tumor lysis Neutropenic Spinal cord

syndrome fever compressio
n

Hypercalcemia SVC
syndrome
Tumor Lysis Syndrome
It is an acute metabolic syndrome caused by the release of
nucleic acids, proteins and intracellular metabolites of
lysed cancer cells in the bloodstream.

It is usually related to bulky, chemo sensitive disease,

including lymphoma, leukemia and germ cell tumors.
More rarely, it can occur spontaneously.
 Tumor cell
Hyperkalemia
lysis

Cardiac arrhythmias

Release of DNA

Purines Hyperphosphatemia

Hypoxanthine/Xanthine Ca-phos precipitation

Xanthine
Allopurinol Hypocalcemia
oxidase

Ur Urate nephropathy
ic
Rasburicase Uricase
aci Ca-phos nephropathy
d
Allantoin
 Clinical Features

• Clinical manifestations may include nausea, vomiting,

somnolence, haematuria, flank pain, oliguria/anuria,
oedema and fluid overload with hypertension, azotaemia,
acidosis, congestive heart failure, muscle cramps, tetany,
syncope, seizures and sudden death.

• They most commonly present within 12–72 hours after the

administration of the cytotoxic therapy.
Diagnosis and Investigations
Prophylaxis against TLS
• Adequate hydration

• Prevent uric acid deposition into renal tubules

• Allopurinol
• Rasburicase

• Urine output monitoring

Management
Adequate hydration: up to 3L/m ,crystalloid saline •
(initial fluid should be free from potassium and
.phosphate)

.Urine out put >100ml/m/hr •

Frequent monitoring of urine out put and electrolytes •

.Diuretics (mannitol or loop diuretics) •

:Treatment of electrolytes disturbance •

hypocalcemia :calcium gluconate
hyperuricemia :Rasburicase

Hemodialysis •
 Hypercalcemia
• Hypercalcemia is defined as
elevated calcium levels in the
blood.it is consider the most
common metabolic disorder in
patients with cancer.

• Most hypercalcemia occur in

multiple myeloma ,breast
cancer and non small cell lung
cancer.
• Parathyroid Hormone-related Protein (PTHrP) over production lead to
hypercalcemia by stimulating osteoclastic bone resorption and increasing renal
tubular reabsorption of calcium.

• 1.25-Dihydroxyvitamin D increasing intestinal calcium absorption.

Clinical features
The symptoms of hypercalcemia are non specific and
:mimic symptoms of underlying malignancy

• Drowsiness
• Confusion
• Nausea and vomiting
• Constipation
• Dehydration
Management
• Diagnosis is made by measuring serum calcium

• Treatment of hypercalcemia based on:

1) Good hydration using intravenous saline 0.9% to increase

calcium excretion and improve renal function.

2) Bisphosphonates (Pamidronate and Zoledronic acid) inhibiting

calcium release by interfering with the metabolic activity of
the osteoclast ( Long acting drugs)
3) Calcitonin intramuscular or subcutaneous to reduce bone
resorption and increase calcium excretion ( rapid acting drug
use in first 24-48h)

4) Dialysis can be considered when hypercalcemia is

accompanied by renal failure.
 Neutropenic fever
• Neutropenic fever is defined as a pyrexia of 38° C for over
1 hour in a patient with a neutrophil count < 1.0 × 109 /L

• Neutropenia is a common complication of malignancy. It

is usually secondary to chemotherapy but may occur with
radiotherapy if large amounts of marrow are irradiated

• Bacterial infections are common in patient with

neutropenic fever but the fungal sources are becoming
increasing prevalent

The risk of sepsis is related to:

1-The severity and duration of neutropenia
2-Intravenous or bladder catheters
Clinical features

1-High fever and affected patients are often non-specifically

unwell.

2- Hypotension is an adverse prognostic feature and may

progress to systemic circulatory shutdown and organ failure.
Investigations

Blood cultures (both peripheral and from central-1

lines if present)
2-Urine culture.
.3- Chest X-ray
.Swabs for culture (throat, central line, wound)-4
High-dose intravenous antibiotics should then be
commenced, pending the results of culture.

1-Typical first line empirical therapy consists of an

antipseudomonal β-lactam (ceftazidime, cefotaxime or
meropenem), or a combination of an aminoglycoside
and a broad-spectrum penicillin with antipseudomonal
activity (gentamicin and piperacillin)

2-Metronidazole should be added if anaerobic infection

.is suspected
3- flucloxacillin or vancomycin or teicoplanin where Gram-
positive infection is suspected.

4-If there is no response after 36–48 hours, treatment should

be recocidered with addition of amphotericin-B or
voriconazole to cover fungal infection.

5-Antibiotics should be adjusted according to culture

results.
 Spinal Cord Compression

• Spinal cord compression complicates 5% of cancers and

is most common in myeloma, prostate, breast and lung
cancers that involve bone.
• The thoracic region is most commonly affected.
 Clinical features

1) The earliest sign is back pain.

2) Sensory changes develop in dermatomes below the level
of compression.
3) motor weakness distal to the block occurs.
4) Sphincter disturbance.
Confirm
diagnosis with
urgent MRI
Management of suspected spinal cord
compression

 Goals of therapy
 Pain control
 Preservation of neuro function
SCC - Therapy
Symptomatic Tx
 High-dose Glucocorticoids
 Ensure adequate analgesia

 Definitive Tx
Neoplasia Score
 Surgery
urgent radiotherapy

The prognosis varies considerably, depending on tumour

type, but the degree of neurological dysfunction at
presentation is the strongest predictor of outcome.
Superior vena cava syndrome
SVC syndrome - Mechanism
• Superior vena cava obstruction (SVCO) is a common
complication.

• causes by neoplastic invasion of venous wall with

associated intravascular blockage. or by extrinsic
compression.

• The most common causes of extrinsic compression are

lung cancer , lymphoma and metastatic tumors.

• Patients with cancer can also develop SVCO due to

intravascular blockage in association with a central
catheter or thromboembolism secondary to the tumor.
Clinical features
The typical presentation is with oedema of the arms and face,
distended neck and arm veins and dusky skin coloration over
the chest, arms and face.

Symptoms
• Dyspnea (63%)
• Facial swelling and head fullness (50%)
• Cough (24%)
• Arm swelling (18%)
• Chest pain (15%)
• Dysphagia (9%)
Physical findings

• Venous distension of neck(66%)

• Venous distension of chest wall (54%)
• Facial oedema (46%)
• Cyanosis (20%)
• Plethora of face (19%)
• Oedema of arms (14%)

Collateral vessels may develop over a period of weeks

and the flow of blood in the collaterals helps to confirm
the diagnosis.
Typical clinical findings in a patient with superior vena cava syndrome

A: Plethora

B: Distended
jugular veins

C: Cyanosis

Swelling .D
hand/arm

Collateral .E
circulation

Compression .F
of SVC/tracheal
compression
Investigations

1-The investigation of choice is a CT scan of the thorax

to confirm the diagnosis and distinguish between
extra- and intravascular causes.
2- A biopsy should be obtained when the tumor type is
unknown.
Treatment of SVC syndrome

Supportive Definitive Treatment

 Elevation of head  Chemotherapy
 Oxygen
 Radiation
 Corticosteroids

 Diuretics
 Stenting, particularly
while bx being pursued
Thank you