Oncological emergencies Flashcards
define febrile neutropenia
an oral temperature of 38.5 degrees C or more, or 2 consecutive readings of 38 degrees C or more for 2 hours, AND an absolute neutrophil count of 0.5X10^9/L or less.
infection responsible for at least half of cases
often no causative organism found-better prognosis, and pt improves as neutrophil count increases
when is febrile neutropenia most often seen?
neutrophil count usually reaches its lowest level 5-10 days after last dose of chemotherapy.
why might a patient having chemotherapy develop neutropenic sepsis but NOT have a fever?*
as pt immunocompromised, there may not be the normal immune response that would cause a rise in temperature
therefore neutropenic sepsis diangosis: pt having anti-cancer treatment with neutrophil count 0.5X10^9/L or less and have either temp higher than 38C, or other signs and symptoms consistent with clinically significant sepsis.
why is early recognition of neutropenic sepsis vital?
deterioration can be rapid and fatal, mortality rate range between 2% and 21% in adults
which patients are at risk of neutropenic sepsis?
those receiving chemo-often 5-10 days after last tment
those receiving extensive field radiotherapy
those with haematological conditions assoc. with neutropenia: leukaemia, lymphoma, myelodysplasia
other causes: non cancer drug related e.g. clozapine, carbimazole, phenytoin, chloramphenicol, infections, hereditary-physiological, autoimmune e.g. felty’s syndrome-RA, splenomegaly, neutropenia.
common organisms involved in neutropenic sepsis?
usually endogenous flora
increasing incidence of gram +ve cocci: staph aureus, staph epidermidis, strep pneumoniae, strep pyogenes, strep viridans, enterococcus faecalis, gram +ve bacillus-corynebacterium
gram -ve: E coli, pseudomonas, klebsiella
fungal infection-candida
what do we want to know in the hx of a pt presenting with suspected neutropenic sepsis?
general symptoms: fever, drowsy, confused
those suggesting underlying infection source: cough, SOB, ENT, dysuria, vomiting, diarrhoea, skin, central line
co-morbidities
Ca type, stage, prior tment and date of last treatment, number of days since last chemo
other drugs: Abx, drugs known to cause neutropenia
signs to examine for in patient with likely neutropenic sepsis?
febrile
tachycardia
hypotension-involve outreach, consider escalation above ward care e.g. ITU admission
dehydration
mouth ulcers
signs of infection: central lines, skin wounds/soft tissue, ENT, chest-creps, SOB, sputum-culture
drowsy, impaired MMSE
investigations to aid initial clinical assessment of pt with likely neutropenic sepsis?
FBC including differentials U+Es, renal profile LFTs, including albumin CRP-note often lags, rise at 48hrs, monitor trend, can be raised in Ca aswell lactate blood culture
further investigations after initial assessment investigations have been performed for neutropenic sepsis?
MSU-culture
stool culture
CXR IF clinically indicated e.g. px cough
clotting-need to assess for DIC-prolonged APTT, decreased fibrinogen, increased FDPs, low PLTs
swabs of lines and wounds
ABG
imaging directed clinically-AXR, CT/MRI-CT abdo if worry about fistulae
NICE recommended empiric ABx therapy for neutropenic sepsis?
IV tazocin (tazobactam and piperacillin) within 1 hour!-given 6hrly (QDS) by IV infusion
if allergy, consider meropenem
if cross reactivity, consider ciprofloxacin (quinolone)
management other than empiric IV broad spec Abx to consider in neutropenic sepsis?
fluid resuscitation
consider catheterisation
consider additional anti-fungal coverage in high risk pts who remain febrile after 3-7 days of BS Abx and no identified causative organism
involve senior team members-SpR and consultant
consider need for care escalation
G-CSF-consider if profoundly septic/neutropenic, may be given prophylactically for future chemo cycles-often given in breast Ca patients having adjuvant treatment, may consider chemo dose reduction if palliative, or stopping the treatment all together.
ensure patients and their carers educated on neutropenic sepsis and how and when to contact 24hr specialist oncology advice and seek emergency care.
give examples of 3 different mechanisms behind SC compression in cancer patients?
extradural spread of a vertebral body metastasis e.g. breast, thyroid, lung, kidney or prostate Ca metastases
or from haematological tumours e.g. multiple myeloma and non-hodkin’s lymphoma
direct metastases e.g. bladder, renal, breast
vertebral crush fracture
importance of a whole spine MRI in investigation of metastatic spinal cord compression?
more than 50% have more than 1 area involved
most common spinal location for metastatic disease?
thoracic spine
which tumours commonly metastasise to bone?
thyroid breast lung kidney-most common metastasis site=lung prostate-note that if pt metastasis of prostate Ca to sites other than bone e.g. lung is very uncommon, bone=most common.
clinical symptoms of metastatic SCC?
back pain-spinal, radicular, worse on coughing and straining, nocturnal pain, spinal tenderness
weakness-difficulty walking, lower limbs giving weigh
sensory disturbance-paraesthesia, anaesthesia
autonomic disturbance-urinary retention, constipation/faecal incontinence
investigations for metastatic SC compression?
MRI WHOLE SPINE
consider targeted CT with 3 plane reconstruction to assess spinal stability and plan vertebroplasty-cement put into the vertebra, kyphoplasty or spinal surgery
myelography-contrast injection in to space around SC and spinal nerve roots
timescale for definitive treatment of metastatic SCC?
24hrs
indications for bisphosphonate treatment to relieve pain in patients with vertebral metastases?
offer to reduce pain and risk of vertebral fracture/collapse when vertebral involvement with breast Ca or myeloma
use to reduce pain in prostate Ca mets only if other analgesia failed
indication for radiotherapy treatment of spinal metastases?
offer 6 Gy single fraction palliative radiotherapy to those with spinal mets causing non-mechanical spinal pain.
treatment of metastatic SC compression?
dexamethasone-at least 16mg PO or IV, give as stat and then 8mg BD with gastroprotection
after surgery e.g. with bone grafting, or start of radiotherapy, should reduce steroid dose gradually over 5-8 days and stop, ensure blood glucose levels monitored whilst on steroids
radiotherapy for definitive treatment-urgent if unsuitable for spinal surgery unless complete tetraplegia or paraplegia for more than 24hrs and pain well controlled, or overall prognosis judged to be too poor.
give post op fractionated radiotherapy to all if satisfactory surgical outcome, once wound healed
offer fractionated as definitive tment if epidural tumour without neurol impairment, mechanical pain or spinal instability.
when should surgery be considered in metastatic SC compression?
if: single vertebral involvement no evidence of widespread disease radioresistant tumour e.g. renal, melanoma to obtain a diagnosis previous RT to site
best outcome for MSCC with surgery and radiotherapy if good pre-op status.
criteria for d/c of patient following neutropenic sepsis?
must be apyrexial for at least 48 hours AND neutrophil count must be more than 0.5 before IV Abx can be stopped-once more than 0.5 can switch to oral e.g. co-amoxiclav.
symptoms and signs of SVC obstruction?
dyspnoea headache visual disturbance swollen face, neck, arms conjunctival and periorbital oedema venous distension in neck and across the chest, pulseless jugular venous distension-fixed raised JVP cyanosis
what definitive treatment is usually given for metastatic spinal cord compression?
surgery, which may be followed with radiotherapy
when would surgery be the only option for patients with metastatic SC compression?
previous radiotherapy to the spine
very unstable vertebral column
when would surgery NOT be used as the definitive treatment for metastatic SC compression?
pt unfit for surgery
pt has very poor life expectancy
how is SVCO differentiated from congestive cardiac failure?
JVP: fixed raised JVP in SVCO, pulsatile in congestive heart failure
hx of heart disease, previous MI
pedal oedema in congestive heart failure
what important differential presents similarily to SVCO?
constrictive pericarditis*
hypercalcaemia presenting features?
abdo pain N+V anorexia weight loss thirst and polydipsia polyuria lethargy bone pain constipation ileus hyporeflexia seizures confusion weakness low mood psychosis bradycardia atrial and ventricular arrhythmias prolonged PR interval
how do skeletal metastases e.g. breast, lung and renal Cas, cause hypercalcaemia?
osteolysis occurs as result of increased osteoclast activity which is due to the tumour cells directly producing RANKL or stimulate bone stromal cells to produce RANKL.
define humoral hypercalcaemia
tumour secretion of PTHrP
3 causes of hypercalcaemia in patients with malignancy?
humoral-PTHrP production by tumour e.g. squamous cell lung Ca, and renal cell carcinoma
osteolytic metastases with local cytokine release
tumour production of calcitriol (active form of Vit D-will increase Ca2+ absorption from the gut)-espec. in lymphomas
investigations in likely presentation of hypercalcaemia?
FBC Us+Es-assess for dehydration LFTs CRP bone profile serum free calcium, ALP, if total calcium need albumin for calcium correction PTH/PTHrP myeloma screen if no known Ca diagnosis CT with contrast chest/abdo/pelvis to investigate metastatic malignancy bone scan
treatment of hypercalcaemia?
aggressive rehydration-IV 0.9% sodium chloride
bisphosphonates-start after 24hrs of IV fluids, e.g. IV pamidronate 60-90mg over 2hrs. can take up to a week to work.
other considerations-calcitonin, corticosteroids
somatostatin analogue e.g. octreotide-reduce PTHrP serum levels
systemic treatment of cancer
how does rasburicase work in the treatment of tumour lysis syndrome?
recombinant urate oxidase
converts insoluble uric acid to allantoin which can be excreted.
define tumour lysis syndrome
series of metabolic treatment complications that occur in rapidly dividing cancers
includes hyperkalaemia, hyperuricaemia and hyperphosphataemia.
which electrolyte is low in the serum in tumour lysis syndrome and why?
Ca2+
from hyperphosphataemia or uric acid nephropathy
tumour types most susceptible to tumour lysis syndrome?
high grade lymphomas e.g. diffuse large B cell, Burkitt's ALL myeloma germ cell tumours small cell lung breast (inflammatory)
patient factors increasing susceptibility to TLS (excluding cancer type)?
prexisting renal dysfunction
hypovolaemia
pretreatment LDH high
urinary tract obstruction from tumour-obstructive uropathy, will cause hydronephrosis.
treatment of persistent anuria in TLS in spite of adequate treatment with hydration, allopurinol and rasburicase?
haemodialysis
how might tumour lysis syndrome present?
normally day 3-7 post chemo:
oliguric/anuric renal failure
lab abnormalities
cardiac arrhythmia/arrest-peaked T waves, QTc derangement
primary presentation of malignancy-spontaneous tumour lysis.
how can tumour lysis syndrome be prevented in the treatment of a pt with high dose chemotherapy for diffuse large B cell lymphoma?
ensure patient adequately hydrated-prescribe IV fluids
give rasburicase or allopurinol, if pt requires rapid reduction in serum uric acid then rasburicase better as serum uric acid is rapidly broken down, whereas allopurinol is inhibiting the formation of uric acid.
supportive care required for the patient with metastatic spinal cord compression?
good nursing care analgesia laxatives bladder care monitors BMs-on steroid treatment VTE prophylaxis physio OT
causes of SVCO?
extrinsic compression: R sided tumours e.g. lung Ca, superior mediastinal lymphadenopathy from rapidly expanding tumours e.g. lymphoma, thymoma and germ cell tumours
intrinsic-thrombosis, FB-?indwelling catheter, tumour
benign causes of SVCO?
aneurysm
goitre
fibrosis
infection
1st signs of SVCO?
puffy neck
non collapsible neck veins
investigations in SVCO?
CXR
gold standard=CT with contrast
?ECHO-worried about constrictive pericarditis
angiography-good for demonstrating degree of compression/collaterals but cannot evaluate extrinsic factors.
evidence of SVCO on CT with contrast?
evidence of extrinsic compression
intraluminal thrombus of SVC
extensive collateralization
treatment of SVCO?
steroids-although no evidence to support use
radiotherapy
chemotherapy-small cell lung Ca, lymphoma and teratoma
stent insertion-rapid relief of symptoms, but not treating the cause
additional management to consider:
anticoagulation
is this a new diagnosis of malignancy?-is there time to take tissue?-if yes then take by safest route, if not consider inserting stent to allow time to obtain tissue.
is this a potentially curative malignancy?-lymphoma curative potential with chemo +/- radio, limited stage small cell can be cured with chemoradiation.
what do you want to include in your examination of a patient with suspected metastatic spinal cord compression?
check for vertebral tenderness lower limb power knee and ankle reflexes plantar reflex sensation check for palpable bladder PR tone
along with urgent MRI spine, what other investigations should be requested in likely presentation of MSCC?
FBC, U+Es, LFTs, Ca, bone profile
must exclude correctable electrolyte imbalance and anaemia
give 4 immediate steps you should take following MSCC diagnosis confirmation?
steroids-PO/IV dexamethasone 16mg stat, then 8mg BD, to reduce any oedema around site of cord compression
analgesics
inform senior
discuss with clinical oncologist regarding urgent radiotherapy or a surgical opinion.
ST toxicities associated with high dose steroids?
insomnia delirium gastric irritation infection-oral candidiasis elevated blood glucose
earliest and most common symptom on spinal cord compression?
back pain
