Haem - Viva - Haem Malignancies Flashcards

1
Q

Why might you admit a haem cancer to ICU

A

May develop critical illness as their first presentation of the disease

May develop complications as part of treatment - chemo, bone marrow etc

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2
Q

Give some causes of critical illness that may be from a haem cancer

A

Neutropenia and sepsis
TLS
GvHD
Resp failure - infection, oedema, haemorrhage, disease infiltration
Complications of chemo
CNS dysfunction - bleeds, thrombosis, hyper viscosity, electrolytes
GI - neutropenic enterocolitis
Renal - nephrotoxics, sepsis, hypoperfusion, underlying disease

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3
Q

Define neutropenia and neutropenic sepsis

A

NICE -
Neutrophil < 0.5 x 10.9/L

Sepsis - Neutrophil < 0.5 plus clinical signs of infection OR temp > 38

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4
Q

Precautions with neutropenic patients

A
Reverse barrier nursing
Positive pressure side room
Avoid invasive procedures - bladder, CVP
Good oral hygeine
Avoid rectal exams/temperature probes (risk of haematogenous spread)
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5
Q

Principles of neutropenic sepsis management

A

ABCDE

Hx - pets and animal exposure, hobbies, recent foreign travel, TB risk, in dwelling lines

OE - oropharnx, skin, perirectoal areas for abscesses

Follow Surviving Sepsis Guidelines, immediate Abx (tazocin)
Bloods including lactate, cultures including in dwelling sites
Fluids and vasopressors

Image, CXR - abdomen CT etc

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6
Q

Empirical Abx for Febrile Neutopenia

A

Tazocin

Consider gentamicin/aminolycosides if gram negative suspected or presence of hypotension or pulmonary infection

Alternative to pen allergy - ciprofloxacin and clindamicin, or vanc and aztreonam

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7
Q

Describe TLS

A

Tumour Lysis Syndrome

Metabolic abnormalities caused by the lysis of a large volume tumour load. Spontaneous or after chemo.
Assoc with leukamias and high grade lymphomas (Burkitts)

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8
Q

Features of TLS

A

High K
High Phosphate
High Uris Acid

High LDH

Low Ca
High Cr
Renal failure
Metabolic acidosis

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9
Q

Treatment of TLS

A

ABCDE

Aggressive fluid resus 
Treat hyperkalaemia (may need RRT)
Rasburicase (recombinant urate oxidase, enzyme with catalyse the oxidation or urate so it can be excreted

Calcium used only for K treatment not to correct a low calcium

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10
Q

Complications of allergenic haemopoiestic cell transplanation

A

Early (<100 days) or late >100 days

Early
Infection
Haemorrhage
Acute GvHD
Aplastic anaemia after graft failure
Late
Chronic GvHD
Chronic pulmonary disease
Infection
Autoimmune disorders
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11
Q

What is Graft versus host disease

A

Immune mediate

Follows allogenic transplant results in complex interaction between donar and recipeint immunity. Antigen presenting cells of recipient interact with the T cells of the donor. Can occur even when donor is perfectly matched and HLA identical.

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12
Q

Features of acute GvHD

A

<100 days

Enteritis
Hepatitis
Dermatitis

Diagnosed by histology or clinically using Seattle Glucksberg Criteria

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13
Q

What is the Seattle Glucksberg criteria

A

Stages acute GvHD

Skin changes, bilirubin level and GI fluid losses (mls/day)

1 - risk under 25% of body. Bilirubin 26-60. GI loss 500-100
2 - Rash 25-50
3 - Rash> 50%, erythroderma
4 - Bullous desquamation of skin. Bilirubin>257, fluid > 2500 with lieu’s

Bilirubin and GI losses increase with each stage

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14
Q

What is chronic GvHD

A

> 100 days
Diverse syndrome resembling auto immune illnesses such as scleroderma, primary biliary cirrhosis, and chronic immunodeficiency. May occur as an extension of acute.

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15
Q

Treatment of GvHD

A

High dose steroids
Immunosuppressants (cyclosporine)
TPN to facilitate gut rest
Octreotide for diarrhoea

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16
Q

What is typhlitis

A

Neutropenic enterocolitis

Life threatening GI complication of chemo

Nause, distension, pain, tenderness, fever, chills.

Needs a CT

Elective right hemi to prevent recurrence.

17
Q

What clinical features would you expect to see with tumour lysis syndrome?

A
  • GI upset, fluid overload.
  • Weakness, paraesthesia, tetany, hypocalcaemia.
  • Arrhythmias — palpitations, chest pain, dyspnoea.
  • Features of renal failure — oligoanuria, haematuria.
18
Q

How would you manage electrolyte derrangement in TLS?

A

hyperuricaemia:
■ xanthine oxidase inhibitors — allopurinol — inhibit uric acid
formation;
■ urate oxidase or rasburicase — increase uric acid oxidation;
- hyperkalaemia:
■ insulin and dextrose, salbutamol nebulizer —shift potassium
intracellularly;
■ calcium gluconate — membrane stabilization;
■ calcium resonium;
- hyperphosphataemia:
■ phosphate binders.