haem emergencies Flashcards
what is neutropenic sepsis
sepsis which occurs with low neutrophill counts
common in those with haem cancers and those un dergoing cancer treatments
Neutropenic sepsis clinical presentation
- neutrophil count <1 x 109/L
- fever >38
- clinical features of sepsis
Neutropenic sepsis risk factors
Anticancer treatment
Haematological malignancy - Particularly acute leukaemias, myelodysplasia, aplastic anaemia
Drugs - E.g clozapine, carbimazole, methotrexate
when Neutropenic sepsis suspected what action do you take
IV BROAD SPECTRUM ANTIBIOTICS WITHIN 1 HOUR + sepsis 6
Do not wait for results in at risk patients!!
Culture EVERYTHING
- Peripheral blood and each line lumen
- Urine
- Viral and bacterial throat swabs
- Sputum if expectorating
- Stool if diarrhoea
- Chest X Ray
sepsis 6
GIVE 3 TAKE 3
1. Oxygen to maintain sats >94%
2. IV access + stat IV antibiotic
3. IV fluids to support BP
- Send bloods inc Hb, lactate
- Send blood cultures
- Monitor urine output – consider catheter
spinal cord compression presenting factors
- Back pain – often severe
- Leg weakness – typically bilateral
- Reduced sensation in legs
- Change in bowel habit
– diarrhoea or constipation - Change in urinary habit
– often retention - Saddle anaesthesia (cauda equina)
name common haematological and non-haematological causes of SCC?
haematological:
- lymphoma (any type but common non-hodgkins)
- myeloma
non-haematological:
- other malignancy
- severe degenerative spinal disease
- disk protrusion
- spinal haematoma
high suspision in those with cancer
what action to take when SSC is first suspected?
- urgent MRI whole spine within 24hrs
- dexamethasone 8mg BD
what to do once its confirmed?
- surgery
- radiotherapy
if haematological:
- bone marrow biopsy - myeloma
- lymph node biopsy - lymphoma
hypercalcaemia presentation
- Onset, pattern/timings
- Headaches
- Limb weakness/altered sensation
- Visual/speech disturbances
- Fevers
- Symptoms to suggest infection?
- Systemic enquiry
- Drugs?
confusion screen for hypercalcaemia
Basic bloods:
- FBC
- U&E
- LFT
- Bone profile
- CRP
- Blood glucose
- B12 and folate
- Thyroid function tests
Consider septic screen:
- Blood cultures, urine culture, CXR
If no clear cause/focal neurology:
- CT head
main symptoms of hypercalcaemia and nemonic
bones, moans, stoans, abdominal groans
bones - increased turnover and fractures
stones - renal stones
moans - confusion, altered mood
abdominal groans - constipation
Hypercalcaemia treatment
- Aggressive IV hydration 2-3L/day
- IV bisphosphonate if Ca > 3 or not responding to fluids
gold standard key diagnostic test for hypercalcaemia
High/High-normal PTH – think parathyroid
Low/low-normal PTH – think malignancy
Other differentials – Vit D excess, drugs, sarcoidosis, other endocrine disorder
most likely haemotological causes in hypercalcaemia
myelomas
lymphomas
tumur lysis syndrome definition
This is a potentially fatal complication of chemotherapy for malignancy (most commonly seen in patient’s with lymphoma or leukaemia).
- rapid breakdown of malignant cells
- occur sponatenously or within first week of steroids or chemo
blood resuts of TLS
Hyperkalaemia
Hyperphosphatemia
Hyperuricaemia
Hypocalcaemia
severe acute kidney injury
how to prevent TLS
- risk assess all patients prior to starting treatment
- hydrate patients
- Allopurinol for most patients – blocks uric acid production
- Rasburicase if high risk
Breaks down existing uric acid
TLS diagnostic criteria
Cairo & Bishop diagnostic criteria
need to have:
- high serum creatine
- arrythmia
seizure
TLS treatment
IV fluids ++++
Rasburicase
Correct high K (not low Ca)
Intensive care for dialysis if not improving
thrombotic thrombocytopenic purpura cause
TTP is caused by ADAMTS13 deficiency
Immune – antibody against ADAMTS13
Congenital (<10%)
TTP pathology
ADAMTS13
Protein which breaks down vWF into smaller multimers
Deficiency leads to build up of large vWF chains
Block vessel lumens
Platelets adhere and aggregate into clots
Red cells can’t pass through – broken down into fragments
what does TTP lead to
Microangiopathic haemolytic anaemia (MAHA)
=intravascular breakdown of red cells
Consumption of platelets
Leads to thrombocytopenia
Build up of clots in blood vessels
Thrombosis -> small vessels – purpura, AKI, neuro symptoms
TTP findings
- low platelets and either MAHA or another feature
- confusion
- large vessel thrombosis
- red cell fragments on blood film
- thrombocytopaenia
