Oncologic emergencies Flashcards
Discuss febrile neutropenia
Historically neutropenia was graded as
- 1-1.5 neturophils mild
- 0.5-1 as moderate
- <0.5 as severe
Mortality reaches 20%
Most common sources are pneumonia, anorectal lesions, skin infections, pharyngitis or UTI. Howevere beacuse local inflammatory response are dampened by the absence of granulocytes the only sign of infection may be fever.
Fever defined as 38.3 or higher or a temperature of>38 for at least 1 hour.
Discuss DDX of fever in the oncology patient
Infection/sepsis
- PE/VTE
- Adverse effect of chemotherapy or other medication
- direct effect of tumor burden
Clear source of infection is identified in only 1/3rd of neutropenic fever cases.
Discuss IX of neutropenic sepsis
2x blood culture
-if pre-existing central access a sample from the line should be taken for culture at the same time as the peripheral ones
Bacterial growth in the catheter 2 hours prior to the peripheral samples is suggestive of a catheter associated infection
Urine, faces and sputum samples should also be sent depending on clinical presentation
CXR
If nil source of fever for 72 hours – ct of chest and sinuses + bronchoalveolar lavage can be considered. Directed CT scan can be performed earlier if clinical signs
Discuss risk of serious complciations with chemotherapy induced neutropenic fever
Any of the following characteristics are considered to be high risk for serious complciations during episdoes of neutropenic fever
1) REceipt of cytotoxic therapy sufficiently myelosupressive to result in anticipated severe neutropenia for >7days
2) MASCC score <21
3) presence of any active uncontrolled comorbid medical problems including
- signs of sever sepsis or septic shock
- oral or GIT mucositis that interferes with swallowing or causes severe diarrhoea
- GIT symptoms including abdo pain, nasuea and vomting or diarrhoea
- intravascular catheter infection especially catheter tunnel infection
- new pulmonary infiltrate or hypoxemia
- underlying chronic lung disease
- complex infection at the time of presentation
4) Alemtuzumab or CAR-T cell use within the past two months
5) uncontrolled or progressive cancer
6) evidence of hepatic insufficiency
Discuss the MASCC score
Risk stratification for the development of complications during neutropenic sepsis
-Age younger than 60 years old -2
-onset of fever while outpatient -3
-overall moderate symptoms burden-3
Absence of dehydration -3
no prior fungal infection or solid tumor type -4
no history of COPD -4
Absence of hypotension -5
Asymptomatic or overal mild symptom burden-5
Over 21 suggest low risk of development of complcations
Discuss management of neutropenic sepsis
ABCD
Antibiotics should be adminsitered within 30-60minutes of presentation and directly after blood cultures have been taken prior to any other investigation.
Monotherapy includes
- PIptaz 4.5 grams QID
- Cefopime
- ceftazodime
- Carbopenums
If line sepsis is a concern add in MRSA cover
-Vancomycin
If in septic shock added additional gram-ve coverage
-gentamycin
Initial coverage for fungal infection is not required unless there is a specific concern for fungal source.
Discuss metastatic spinal cord compression
Malignancy related compromise of the spinal cord most commonly occurs from an extradural neoplasm that has haematological metastasized to the vertebral column. Lesion then typically expands locally from the marrow space through a veterbal vein foramen to invade the spinal canal
Although termed spinal cord compression direct nerve compression by the tumor is rarae. Cord injury is more commonly cuased by occlusion of the epidural venous plexus leading to breakdown fot he blood cord barreir and vasogenic oedema. If untreated eventually leads to occlusion of the arterial system leading to cord ischaemia and infarction.
Most common tumors causing MSCC are prostate, breast and lung cancer.
RCC, non hodgkins lymphoma and multiple myeloma each account for additional 5-10% of all cases.
Most cases affect the thoracic spine (60%) followed by the L spine (25) and c-spine (15%)
Discuss clinical features of MSCC
Back pain, weakness, sensory loss and autonomic funciton loss are the most frequent presenting complatins.
Back pain occurs in more than 95% of pateitns
Extremity weakness occurs in 75% of patient and generally preceeds sensory loss
ANS dysfunction is present in 60% of cases includ9ing loss of bowel or bladder function
Discuss IX of MSCC
MRI is gold standard if MSCC is suspected with a sensitivity of 93% and specificity of 97% - even if MSCC has been confirmed by another imaging modality MRI should be performed as its added resolution changes treatment strategy in approximatly 50% of cases
THere is a 20-40% of multiple seperate lesions as such the L, t and C spine should all be imaged
If MRI unavailable or contraindicated CT is the next imaging modality of choice - IF vertebral metastasis is seen on initial scanes presence of cord comrpession can be assessed by CT myelography in which contrast is introduced into the subarachnoid space.
DIscuss management of MSCC
Corticosteroids and initiation of surgery or radiation or both.
Steroids provide the most immediatlely aviable therapy for cord compression. Early steroids have been shown to improve ambulation rates at 3-6 months and improved long term pain scores.
10mg of IV dexamethasone followed by 16 mg orally daily in divided doses for any patient with neurological deficit secondary to MSCC.
Patients with severe deficiencies such as paraplegia may receive higher doses of 100mg IV dexamethasone followed by 96mg orally daily in divided doses.
Steroids temporize vasogenic cord oedema but cord damage will ensure without definitive treatment with radiation and surgery.
30 day mortality rates for spinal cord decompression exceed 10% and complications rates exceed 50%. For patient not fit for surgery or with incompatible goals radiation therapy alone should be offered
If surgery is to be offered it should be done prior to radiation to reduce risk of non healing wiunds
NO evidence for timing but experts recommend definitive treatment within 24 hours.
Discuss malignant pericardial effusion
Pericardial manifestation of malignant disease including pericarditis, neoplasm (normally metastatic) and pericardial effusion effect greater than 10% of cancer patients and cause about 25% of all effusive pericardial disease in the developed world.
2/3rd asymptomatic
1/3 HD compromise, organ failure and death can occur
Neoplastic disease is belived to cause pericardial effusion when lymphatic flow which normally drains fluid fro the pericardium becomes obstructed or reversed by congestion in porximal malignant lymph nodes.
Most common causes of metastatic spread are lung, breast and haematological tumors
Although the pericardial sac has the elastic potential for gradual expansion to more than 1 l its is poorly distensible in short (hours to days) time frames and rapid accumulation of ever a few hundred millilitres of fluid may precipitate cardiac tamponade
Discuss clinical features of malignant pericardial disease
Dyspnoea and chest pain
Weakness and fatigue are often associated and large slowly accumulating effusions may result in mass effect on nearby structures, causing nasuea, early satiety, cough hiccups hoarsenss or dysphagia.
Tamponade present with shock but other classic stigmata are unreliable
- Pulsus paradoxus - defeined as a 10mmhg systolic BP gradient between inspiration and expiration in the respiratory cycle is the most sensitive sign
- Kassmausl sign (paradoxical increase JVP with inspiration)
- Becks triad - hypotension, elevated JVP and mufffled heart sounds
Discuss management of malignant pericardial effusions
Usually indicates advanced cancer and management should be tailored to the patients wisehs and management plan.
If agressive therapy is wanted tamponade is a medical emergency and warrants immediate drainage, ideally under real time US guidance.
US pericardialcentesis via the intercostal approach resuolts in fewer compications and higher success than the blind subxiphi approaxh.
BLind technique
- semirecumbent
- needle inserted subxiphoid
- angle of 15 degrees to the horizntal between the xiphoid and left sternal margin
- after clearing trhe ribs the needle should be leveled and advanced toward the left shoulder until return of fluid is achieved.
Temporising measures such as IV fluid to increase preload and inotropes (epi, dobutamine) may be attempted
Effusion wihtout tamponade can be managed non emergently - fluid sampling and intrapericardial chemo or injection of sclerosing agents in more controlled fashion
Discuss pathophysiology of hypercalcaemia in the cancer patient
Serum calcium regulation is achieved by PTH and calcitriol which both increase serum calcium level and to a less extent by calcitonin which decreases it.
Approximatly 30% of cancer patient will experience dysregulation of calcium homeostasis usually caused by 1 or more of the following
1) Synthesis of PTH analog PTH related protein
2) Overproduction of calcitriol
3) bone osteolysis due to direct spread of tumor
4) ectopic PTH production.
In most cases malignancy associated hypercalcemia signifies advanced disease with a median survival of less than 2 months.
Discuss clinical features of hypercalcaemia
- Bones (increased osteolysis and fracture)
- Stones (renal colic)
- psychic Moans (depression, confusion, hallucinations and coma)
- abdominal Groans (Anorexia, N&V, consiptation, PUD, pancreatitis)
Other
- muscle weakness, malaise, hyporeflexia
- nephrogenic diabetes insipidus (polyuria and polydipsia)
Complications
-cardiac arrythmias (AV block, arrest)
