Onco Emergenices (Secondary To Cancer) Flashcards
What cancers are most likely to get bowel obstruction as a complication?
how does it happen?
- Complication of advanced cancer
- Cancer in abdomen
- Ovarian (40%)
- Bowel
- Stomach cancer
- Metastasis
How?
* Cancer grows into nerve supply of bowel and stops muscles working
* Adhesions due to past abdominal surgery
How does bowel obstruction present?
- Stomach pain- colicky
- Constipation - absolute no wind
- Vomiting
- Occurs early in upper GI obstruction and later in lower GI
- Abdominal distension
- bloated
- tinkling bowel sounds -early
Investigations for bowel obstruction?
- Abdominal X ray: distended loops of bowel.
Central- upper
Peripheral- lower - CT scan
- Barium enema
normal limits : 3 cm small bowel
6 cm colon
9 cm caecum
Supportive management of bowel obstruction?
If able to go to theatre:
* NBM
* NG decompression/ venting gastrostomy (PEG)
* IV fluids to prevent dehydration
A lot of patients will not be able go to theatre:
* steroids- to reduce odema of bowel wall
* gentle laxatives and anti-emetics- to control N&V
* Control the pain
* reduce volume of intestinal secretions
Medical management of bowel obstruction?
- Buscipan- stop muscle spasms and reduce pain
- Strong painkillers
- IV antibiotics
- Antiemetics
- Octreotide -Reduces fluid that building up in GI tract
- Steroids to reduce inflammation in bowel
Surgical management of bowel obstruciton in oncology?
Tends to be palliative to relieve pain:
- Resection of damaged bowel-> stoma
- Stent insertion
Why might a pt with bowel obstruction become unstable?
complications of bowel osbtruction
- Hypovolaemic shock due to fluid stuck in the bowel rather than the intravascular space (third-spacing)
- Bowel ischaemia
- Bowel perforation
- Sepsis
Full set of bloods is suspect bowel obstrutction: what KEY results expect to find?
- Electrolyte imbalances (U&Es)
- Metabolic alkalosis due to vomiting stomach acid (venous blood gas)
- Bowel ischaemia (raised lactate – either on a venous blood gas or laboratory sample)
causes of Superior vena cava obstruction?
malignant and non malignant
Malignancy
* Primary lung cancer e.g. Pancoast tumour
- Small cell
- Non small cell e.g. Squamous (pancoast)
* Lymphoma
* Metastasis
* Kaposi’s sarcoma
* breast cancer
Non malignancy
* aortic aneurysm
* mediastinal fibrosis
* goitre
* SVC thrombosis
Pathophysiology of superior vena cava obstruction
- The SVC provides venous drainage for the head, the neck, the upper extremities and the upper thorax
- Tumour presses on SVC
- Less blood draining from veins in the brain into the heart
Presenentation of SVCO?
- Tachycardia, tachypnoea, hypotension
- Oedema and errythema of the upper body, extremities and face
- Jugular venous distension
- Dilated veins over the arms, neck and anterior chest wall (collaterals )
- Pemberton sign - positive
- Engorged conjunctiva.
- Convulsions and coma.
- Cyanosis.
- Severe respiratory distress.
How to ellicit Pembertons sign?
- Ask patient to raise both arms above head (2-3mins)
- Normal result: nothing happends
- SVC syndrome present: facial and neck swelling, cough, SoB, cyanosis
Investigation for SVCO
- CXR -widened mediastinum or a mass on the right side of the chest.
- Doppler scanning: changes seen during the respiratory cycl, evaluate the severity and effect of therapy
- CT scan with contrast - gold standard
- detect effusions, metastatic intra- and extrapulmonary manifestations, assessment of collateral vasculature and planning of interventional procedures.
Complications of SVCO
- laryngeal oedema causing laryngeal constriction
- Tracheal obstruction
- Resp distress
- Hypotension (reduced cardiac output) and tachycardia
- Cyanosis
- Retinal haemorrhage
- Stroke
- Cerebral oedema
Management of SVCO
- Head elevation, 02
- Corticosteroids, diuretics
- Endovascular surgery - stenting
Palliative care
* Cryotherapy
* Diathermy
* Bronchial stents for central airway
* Endobronchial radiotherapy
How is hypercalacaemia defined?
Hypercalcaemia is defined as correct calcium >2.65mmol/L.
(Normal range 2.2-2.51 mmol/l)
Ca and albumin link
Can be free or bound to albumin
* Adjusted for how much albumin in blood
* If low albumin – may be low calcium as decreased binding of calcium
What are common causes of hypercalcaemia related to malignancy?
- often in disseminated disease- poor prognosis
- Humoral cause (80%) (tumour derived PTHrP)
- Bone invasion
- myeloma
- Tymour calcitriol release
- immunotherapies and hormonal therapy
non malignancy causes of hyercalcaemia?
- Primary hyperparathyroidism
- Granulomatous diseas : sarcoidosis/ TB
- vitamin D intoxication
- acromegaly
- thyrotoxicosis
- Milk-alkali syndrome
- drugs: thiazides, calcium-containing antacids, Lithium
- Addison’s disease
- Paget’s disease of the bone
humoral cause of hypercalcaemia?
(blood related - relating to, proceeding from, or involving a bodily humor (such as a hormone))
- PTH-related protein released by certain cancers
- E.g. paraneoplastic feature of lung cancer – SCC
- Increased release of calcium from bone and increase uptake from kidneys
Risk factors for hypercalcaemia?
(i.e. which malignancies can cause high calcium)
Breast cancer
SCC (NSCLC)
Renal
Myeloma
Lymphoma
How does bone invasion cause hypercalcaemia?
Osteolytic metastases with local release of cytokines -> increased bone reportion and therefore calcium release from bone into blood
Presentation of hypercalcaemia?
Bones, stones, groans and psych moans (painful bones, kidney stones, abdominal groans and psych moans)
* Nausea
* Anorexia
* Thirst
* Constipation
* Kidney stones
* Confusion
* Polydipsia and polyuria
* Fatigue and weakness
* Bone pain
* Neurological
* Cardiac
hypercalcaemia and neurological symptoms?
(what neurological symptoms present with hypercalcemia?)
Seizures
Poor coordination
Change in personality
cognitive dysfunction
depressin
hypercalcaemia and cardiac symptoms?
Bradycardia
HTN
Shortened QT interval
Revision calcium homeostasis
Reduction in calcium detected by the PTH gland
* Increase PTH secretion
* Increase PTH in plasma
reabsorption of Ca from bone – increases plasma Ca2+
Kidney:
* Calcium reabsorption in nephron increases
* Reduced excretion of calcium
* Reduced reabsorption + increased excretion of phosphate
o Low plasma phosphate= higher calcium in plasma (inversely proportional)
Vitamin D
* PTH increases 1,25 dihydroxycholecalciferol (active vitamin D ) in the kidney
* more Ca absorption from intestine
* Increase plasma calcium
RESULT:
Restore plasma calcium to normal – negative feedback to PTH gland
How does calcitonin effect ca?
a peptide released from the thyroid- has an opposite effect to PTH
- when PT detects high calcium- calcitonin released
Investigations of hypercalcaemia ?
- ECG
- LFTs
- U+Es
- Bone profile (calcium, phosphate, albumin, total protein, ALP)
- PTH (parathyroid hormone)
Further investigation depends on the suspected diagnosis:
* Urinary Bence-Jones proteins and plasma electrophoresis (for myeloma)
* FBC (myeloma)
* Chest x-ray (myeloma, sarcoid, TB)
* 24 hour urinary calcium (familial hypocalciuric hypercalcaemia)
* Bone scan/PET Scan (malignancy)
* USS neck
ECG findings in hypercalcaemia?
- Osborn wave
- ST segment elevation
- Biphasic T waves
- Prominent U waves
- Shortened QT interval
How is hypercalcaemia managed?
Treating the immediate complications and reduce calcium release into the blood:
- Aggressive IV fluids - 3-4 litres/day. (corrects dehydration, protects the kidneys and increases calcium excretion)
- Bisphosphonates
* (inhibits osteoclast activity reducing calcium release)
* e.g. IV pamidronate or zolendronic acids - renal failure so must ensure properly rehydrated first
* Denosumab for refractory hypercalcaemia - Further management to prevent recurrence (depending on the cause):
* Chemotherapy (malignancy)
* Surgical resection (malignancy)
* Radiotherapy (malignancy)
* Steroids (sarcoidosis)
* Calcitonin
* Furosemide - reduce reabsortion of calcium
VTE and malignancy
common?
why do they happen in malignancy?
RIsk for cancer vs other patients?
- VTE in cancer patients is a common cause of mortality
- Hypercoagulable state is a hallmark of cancer
- Increased risk 2-3X the normal population
- Complicated managing risk of thrombocytopenic bleeding and risk of clots
- People with cancer who undergo surgical resection are at higher risk than patients who undergo surgery for non-malignant disease
Pathophysiology of VTE and malignancy
Hypercoagulable state induced by specific prothrombotic properties of cancer cells that activate blood clotting
Activation of:
* Platelets
* Leukocytes
* Endothelial cells / damage
endothelium activation by anti-cancer drugs
High risk cancers for VTE?
Pancreatic
Gastric
Lung cancers
Patient and cancer treamtent RF for VTE?
Patient RF
* CVD
* Smoking
* Obesity
* COCP/HRT
* inactivity / immobility
Cancer treatment RF
* Cisplatin
* Tamoxifen
Presentation of VTE
DVT
* Redness
* unilateral warm, swollen calf or thigh
* Tenderness
* pain on palpation of deep veins
* Pitting oedema
* Collateral superficial veins
PE
* SoB
* Chest pain
* Cough
* Tachycardia
* Cyanosis
* Dizziness and fainting
* sweating
investigations for VTE
- D-dimer raised in cancer so not used as a predictor
- DVT- US of leg
- PE- CTPA
AR of Wells Score for DVT
Wells score for DVT result that makes DVT likely
2 or more = DVT likely
1 or less = DVT unlikely
Management of VTE
DOAC +/- LMWH, warfarin, LMWH alone
DOACS
* Apixaban
* Rivaroxaban
* Dabigatran
* Edoxaban
LMWH
* Dalteparin
* Enoxaparin
Pt w/active cancer should be anticoagulated for at least 3-6 months. Unprovoked DVTs 6 months
DR Barbara said - she would do LMWH as easier to reverse than DOAC. Safer.
Reducing risk of blood clots whilst in hospital
- Anticoagulants
- Antiembolic stockings
- Compression devices
- Keeping moving
- Stopping COCP or HRT
- Keeping hydrated
GI bleeding and cancer: what patients get it?
- patients with solid cancers and also those with bone cancers due to thrombocytopenia
- Problem in advanced cancers mostly
- Divided into Upper and lower GI bleed
Causes of bleeding secondary to cancers
- Local tumour invasion
- Thrombocytopenia
- Abnormal tumour vasculature
- Oesophagitis secondary to radiation
- Liver cancer- portal hypertension (oesophageal varices)
- Tumor regression
- Radiation or chemotherapy or immunotherapies
- Steroid therapy
Causes of upper GI bleed?
- Gastric ulcer (splenic artery erosion)
- Duodenal ulcer
- Oesophageal varices
Presentation of upper GI bleed?
Haematemesis
* Coffee ground vomiting- digested blood
Melaena
* tar like, black greasy and offensive stools caused by digested blood- oxidised
Haemodynamic instability
Epigastric pain
raised urea
Tacchy / hypovolaemia
Scoring systems for Upper GI bleed
Glasgow-Blatchford score and Rockall
When is the Glasgow- blatchford score used?
It scores patient based on their clinical presentation with upper GI Bleed.
The Glasgow-Blatchford score is preferred by NICE pre-endoscopy for deciding upon timing of the procedure.
used to plan: e.g. those scoring<0 may be suitable for outpatient OGD
What parameters does the Galsgow blatchford score look at?
- Urea
- Haemoglobin (different for men and women)
- Systolic blood pressure
Other paremeters:
* Tachycardia
* Clincally observed malaena
* Syncope
* Liver disease
* Heart failure
When is Rockall score for upper GI bleed used?
Used in pts that have had an endoscopy to calculate their risk of rebleeding and overall mortility
What parameters for the Rockall score look at?
Compare Glasgow - blatchford and Rockall scores
Glasgow- blatchford
* establishes risk of having an upper GI bleed in order to make a plan e.g. discharge them or not
Rockall
* calculates risk of rebleeding and overall mortality
Management of an upper GI Bleed
ABATED
A – ABCDE approach to immediate resuscitation
B – Bloods / fluids
A – Access (ideally 2 large bore cannula)
T – Transfuse (group and save, if varices 4 units blood cross-matched))
E – Endoscopy (arrange urgent endoscopy within 24 hours)
D – Drugs (stop anticoagulants and NSAIDs)
Bloods:
* Haemoglobin (FBC)
* Urea (U&Es)
* Coagulation (INR, FBC for platelets)
* Liver disease (LFTs)
* Crossmatch 2 units of blood
* Transfusion blood, platelets (if <50) and prothrombin complex concentrate (if on warfarin) in patients with massive hameorrhage
Definitive investigation/treatment:
* Esophagogastroduodenoscopy (OGD) (within 12h)– stops bleedings
V PPI may also be initiated.
In variceal bleeding, IV terlipressin and a
GI Ulcers
Pathophysiology
Erosion of blood vessels supplying upper GI tract
- Lesser curve of stomach (20%)
- Posterior duodenum (40%)
Gastroduodenal artery most common
RF for ulcers?
Ulcer disease
H pylori positive
NSAIDS
Steroids
Investigations for ulcers?
(peptic ulcer)
Erect CXR if suspect peptic ulceration
Management of peptic ulcers
- A to E
- Injection of adrenaline and cauterisation of bleeding
- High dose IV PPI therapy (e.g. IV 40mg of omeprazole) to reduce acid secretion
- +/- H.Pylori eradication therapy if necessary
What is oesophagitis?
Inflammation of intraluminal epithelial layer of the oesophagus
Causes of oesophagitis ?
- GORD
- Infections e..g candia albicans
- Medication (bisphosphonates)
- Radiotherapy
- Ingestion of toxic substance
- Crohns disease
Pathophysiology of oesophageal varicies
- Dilation of portosystemic venous anastomoses in oesophagus
- portal HTN
- Thin, swollen and dilated- prone to rupture
Risk factors for oesophageal varices
- Alcoholic liver disease
- liver cancer or metastatic liver cancer
Risk factors for oesophageal varices
- Alcoholic liver disease
- liver cancer or metastatic liver cancer
Variceal rupture management
- ABC
resuscitation before endoscopy i.e. blood transfusion - correct clotting: FFP, vitamin K, platelet transfusions may be required
- vasoactive agents: terlipressin
- prophylactic IV antibiotics- quinolones
- Endoscopy: endoscopic variceal band ligation
- Sengstaken-Blakemore tube if uncontrolled haemorrhage
- Transjugular Intrahepatic Portosystemic Shunt (TIPSS) if above measures fail (connects the hepatic vein to the portal vein exacerbation of hepatic encephalopathy is a common complication_
Lower GI bleeding main symptoms?
rectal bleeding (haemtochezia)
- passage of fresh blood per rectum
causes of lower GI bleed
- Ischaemic or infective colitis
- Haemorrhoids
- Malignancy
- IBD
- Radiation proctitis
- Diverticular disease
History taking for lower GI bleed
- Nature of bleeding, including duration, frequency, colour of the bleeding, relation to stool and defecation
- Associated symptoms, including pain (especially association with defaecation), haematemesis, PR mucus, or previous episodes
- Family history of bowel cancer or inflammatory bowel disease
Examination for lower GI bleed
abdomen
* localised tenderness / masses palpable.
PR examination
* every patient presenting with haematochezia
* assess for any rectal masses and ongoing presence of blood
Investigation for lower GI bleed
- Bloods- FBC, U&Es, LFT, clotting
Acute bleed may not show reduced Hb levels - Group and save
- Stool culture
Haemodynamically unstable:
* stabilise before undergoing urgent CT angiogram to find source of bleeding
Haemodynamically stable:
* Flexible sigmoidoscopy (exclude left colonic pathology)- can be outpatient
PR bleeding but no abnormality found on colonoscopy
* look for upper GI bleed- OGD
management of unstable lower GI bleed
Standard A to E
- IV fluid
- Blood products
- Hb <70 requires transfusion of packed red blood cells (unless pt has CVD, then Hb <80 used)
- Reversal of any anti-coagulation
Potential management
* Endoscopic haemostasis methods -Injection (diluted adrenaline)
* Mechanical therapies (endoscopic clips and band ligation)
* Arterial embolization possible in those with identified bleeding point (termed a ‘blush’ of sufficient size on angiogram
**Surgery **
* Rarely required
* May be considered in pt with ongoing GI bleeding (requiring continued transfusion), where endoscopic and radiographic treatment has failed
What is ascites?
Pathological accumulation of ascitic fluid in the peritoneal cavity
Peritoneum makes up ascitic fluid -> if it builds up -> ascites
Causes of ascites?
- Portal hypertension (cirrhosis, heart failure, liver cancer)
- Non-portal hypertension
–> Hypoalbinemia, malignant, infection
Pathophysiology of ascites in cancer patients
Cancer of the liver
* Portal HTN forces fluid out of nearby blood vessels
* Damage to the liver reduces albumin production -> reduced hydrostatic pressure
Metastasis to the peritoneum
* Makes it leaky- malignant ascites
presentation of ascites
- Swollen / distended of the abdomen
- Tightness
- Feeling full when eating
- Nausea
- SoB
If infected
* Pain
* Fever
* rigors
investigations for ascites?
- US
- Needle aspiration- paracentesis
Looking for: WBC, blood, cancer cells, bacteria - serum ascites albumin gradient (SAAG) to determine cause (subtract the ascitic albumin concentration from the serum albumin concentration.)
- Examination- shifting dullness
SAAG > 11g/L (indicates portal hypertension) e.g. cirrhosis .<11g/L - hypoalbuminaemia, malignant peritoneal
The causes of ascites can be grouped into those with a serum-ascites albumin gradient (SAAG) <11 g/L or a gradient >11g/L .
Give causes of ascites with HIGH serum- ascites albumin gradinet and LOW
Management of ascites?
- Address the underlying cause
- Salt restricted diet
- Fluid restriction
- Spironolactone
- diuretic e.g. furosemide if spironolactone is insufficient.
- refractory acites -therapeutic paracentesis- fluid is drained from the abdomen over a few hours.
- prophylactic antibiotics to reduce the risk of spontaneous bacterial peritonitis e.g. oral ciprofloxacin
What is a plueral effusion?
Pathological accumulation of pleural fluid in the pleural cavity
Causes of plueral effusion
Lung infections
Heart failure
Metastatic cancer
* Lung cancer
* Breast cancer
* Ovarian cancer
* Lymphomas
Primary cancers
* Mesothelioma (cancer of the pleura)
Presentation of pleural effusion
presnting and examination signs
- Breathlessness
- Cough
- Chest pain
Examination
* Stony dullness
* Trachea pushed away from effusion
Investigations and definitive diagnosis for pleural effusion
- Chest X-ray
- Test fluid for: WBC, cancer cells, culture for bacteria
- ECG
- Bloods: FBC, U&E’s, LFT’s, CRP, Bone profile, LDH, clotting
- ECHO (if suspect heart failure)
- Staging CT(with contrast) if suspect exudative cause
Definitive diagnosis
* US guided pleural aspiration -
Biochemistry (protein, pH, LDH, Cytology, Microbiology)
* If no tracheal deviation then pathology may be a mixture of atelectasis and effusion (pull + push = no deviation)
* Bedside US to determine if fluid or collapse
Caution when managing a pleural effusion?
- Never inset a chest drain unless diagnosis is well established e.g. known metastatic lung cancer
- draining fluid may hinder opportunity to obtain pleural biopsies
Management of plueral effusions
complications as well
- Chest drain
* Complications: blocked drain, infected drain, pneumothorax, recurrence - Management of Recurrent plueral effusions :
* Catheter insertion
* Pleurodesis –> Fusion of 2 pleural layers
Management of plueral effusions
complications as well
- Chest drain
* Complications: blocked drain, infected drain, pneumothorax, recurrence - Management of Recurrent plueral effusions :
* Catheter insertion
* Pleurodesis –> Fusion of 2 pleural layers
Causes of Transudate effusions (pleural protein <30 g/L)
Common:
- Heart failure
- Cirrhosis
- Hypoalbuminaemia (nephrotic syndrome or peritoneal dialysis)
Less common:
- Hypothyroidism, mitral stenosis, pulmonary embolism
Rare:
- Constrictive pericarditis, superior vena cava obstruction, Meig’s syndrome
Causes of Exudative effusions (pleural protein >30 g/L)
Common:
- Malignancy
- Infections – parapneumonic, TB, HIV (kaposi’s)
Less common:
- Inflammatory (rheumatoid arthritis, pancreatitis, benign asbestos effusion, Dressler’s, pulmonary infarction/pulmonary embolus), Lymphatic disorders, Connective tissue disease
Rare:
- Yellow nail syndrome, fungal infections, drugs
Lights criteria for plerual effusion : transudative or exudative
Why might a cancer pt get raised ICP
Principle cause of RICP in cancer patients is
- Space-occupying tumour
- Obstructive hydrocephalus
Presentation of a SOL
- N and V
- Dizziness
- Changes in eyesight
- Behaviour changes
- Worse on cough
- Worse on leading forwards
Neurological problems:
* Eyesight
* Weakness and numbness
* Coordination problems
* Arthralgia
* Reduced consciousness
Coning symptoms- emergency
* Bradycardia
* High blood pressure
* Abnormal breathing
Investigations of RICP
CT scan +- MRI with and without contrast
Fundoscopy
- Papilledema
- Loss of retinal venous pulsation
Lumbar puncture-> to determine CSF pressure and look for cancer cells
Management of RICP
Dexamethasone to shrink tumour
Antibiotics if infective cause
Cancer treatment if SoL:
* Debulking surgery
* Radiation therapy
* Intrathecal chemotherapy- given via lumbar puncture
Surgery:
* Cerebral shunts placed tp drain CSF and lower ICP
* CSF is drained from brain to the abdomen
Why are cancer pts at greater risk of seizures?
epileptic seizures increase in cancer patients due to
* Brain metastases and
* Primary brain tumour
How is status epilepticus defined?
Status epilepticus is defined as:
* a single seizure lasting >5 minutes, or
* >= 2 seizures within a 5-minute period without the person returning to normal between them
Risk factors for status epilepticus in cancer pts
- Slow growing , low grade tumour
- Tumour is in one of the lobes of the cerebrum or meninges
Pathophysiology of status epilepticus in cancer pts
- Due to abnormal development of cells around the tumour
- May be due to imbalance of chemicals in the brain caused by tumour
- Leads to altered electrical activity in the brain -> epilepsy
managemetn of frequent seizures in cancer patients?
Management
* Anti-epileptics
Frequently used anti-convulsants include:
* levetiracetam (Keppra®)
* sodium valproate (Epilim®)
* lamotrigine (Lamictal®)
* clobazam
* carbamazepine (Tegretol®)
* topiramate
* phenytoin (Epanutin®).
Surgery- neurosurgery
status epilepticus emergency management
Start timer
1) After 5 mins give
- Lorazepam IV or if in community midazolam buccally/rectally
2) After 10 mins
- Lorazepam IV
- Prepare second line medication
3) At 15 mins
- Levetiracetam
- Phenytoin
- Phenobarbital
4) At 20 mins
- Intubate or administer further alternatives to the second line drugs (Levetiracetam, phenytoin, phenobarbital)
5) If this does work
Rapid sequence induction of anaesthesia using thiopental sodium
What is? metastatic spinal cord compression? (MSCC )
how many people does it affect? where exactly is cord compressed?
- Spinal cord compression is an oncological emergency and affects up to 5% of cancer patients.
- Extradural compression accounts for the majority of cases, usually due to vertebral body metastases.
- Increasingly common due to prolonged survival
Which cancers have highest risk of Metastatic spinal cord compression (MSCC )
- lung
- breast
- prostate cancer
Pathophysiology of MSCC
and causes, mets from which cancer?
Occurs when dural sac and its contents are compressed at the level of the cord or cauda equina
Causes
* Collapse of vertebral body due to bony mets causing brittle bones
* Metastasis in the epidural space (paraspinal area)
–> Especially lymphoma
Stages of damage to the spinal cord in MSCC
1) Reversible initial stages
- Initially oedema
- Venous congestion
- Demyelination
2) Prolonged compression
- Vascular injury
- Cord necrosis
- Permanent damage
Presentation of MSCC?
- Back pain
- Motor symptoms (upper motor neuronee signs)
- Sensory loss
- Sphincter dysfunction
- Diminishing performance status/generally unwell
Presentation of MSCC: back pain
elaborate on its features
- Often for 2-3 months
- Poorly responsive to analgesia
- Radiation around chest- band like
- Radicular –> Exacerbated by neck flexion, SLR, coughing, sneezing, straining
- Pain at night/ wakes up
Presentation of MSCC: motor symptoms
elaborate on its features
- (upper motor neuronee signs)
- Affects >75%,
- Reduced power, difficulty standing, walking, climbing stairs, often symmetrical
- (high cervical scc causes poor truncal balance)
Presentation of MSCC:
Sensory loss
how common?
Affects >50%, but may be unaware until examined
Presentation of MSCC: Sphincter dysfunction
elaborate on its features
- Urinary hesitancy, frequency, then urinary retention with overflow, faecal incontinence
examination findings of a patient with MSCC?
- Acute onset -> Flaccid paralysis
- Progressive (UMN):
a. - Spasticity (increased tone, clonus, hyperreflexia in limbs below level of MSCC)
b. - Plantar reflexes up-going - Babinski (not cauda equina- LMN)
c - Palpable bladder (urinary retention)
d. - Sensory loss with well defined dermatomal levels - Cauda equina
Common areas of spine involved in MSCC?
- Thoracic commonest site
- 30-50% - >1 areas involves
- Below L2 vertebra= cauda equina(compression of peripheral nerve and not spinal cord)
investigation for MSCC?
- MRI of the whole spine
- Routine blood
- If high chance of surgery- Group and save and clotting screen
When to refer if suspect MSCC>
Referral
- Pain suggestive of spinal mets – MRI within 1 weeks
- Signs MSCC, MRI within 24 hours
UMN vs LMN signs
UMN
- Spinal cord compression
o Hypertonia
o Hyperreflexia
o Babinskis sign
o clonus
LMN
- Cauda equina
- Peripheral nerve compression
Initial management of MSCC?
- Admit and treat within 24 hours of diagnosis
- Bed rest / log-roll (preserve spinal stability and prevent neuro deterioration)
- Dexamethasone 16mg + PPI
- Adequate analgesia
If >48hrs no motor function -> supportive care
- Analgesia
- Laxative
- Care of pressure areas
- Bladder
- Monitor BMs
- VTE prophylaxis
- Physiotherapy
- OT
Surgical management of MSCC?
first line surgery , best suited for which cancers?
Surgery
- First line treatment- Balloon kyphoplasty
Best suited:
* Multiple myeloma
* Lymphoma
* Breast
* Prostate
* Renal
Which patients are good candidates for surgery for MSCC?
AIM of surgery
Good motor function at presentation
* Good performance status
* Limited comorbidity
* Single level spinal disease
* Absence of visceral mets
* Long interval from primary diagnosis
* Helpful for biopsy/ stabilisation
Aim:
* Relive compression
* Remove tumours
* Stabilise spine
* Preserve greater degree of mobility
What partients recieve radiotherapy for MSCC?
How does it work?
- Majority receive this (due to extensive disease- multi spinal level disease, mets and/or compression and poor performance status when MSCC occurs)
- Delivered within 24 hours
MOA:
- Targets abnormal area plus 1-2 vertebra either side
Aim of radiotherapy for MSCC?
life expectancy ?
- Relieve compression of the spine and nerve roots by causing cell death in the rapidly dividing tumour tissue
- Relives pain and stabilises neurological deficict
- Life expectancy often measured in months
When might chemotherapy be considered for MSCC?
Urgent chemotherapy
- May be considered if very sensitive tumours e.g. lymphoma /SCLC
Causes of cauda equina?
Causes
- Disc herniation
- Trauma
- Neoplasm
a. Primary or metastatic:
b. Most common cancers that spread to spinal vertebrae: thyroid, breast, lung, renal and prostate)
- Infection
- Chronic spinal inflammation
- Iatrogenic
Where does the lesion have to be to be called cauda equina? what fibres involved?
Caused by compression of the spinal cord
- Below L2
- Peripheral nerves (LMN), containing motor and sensory fibres
presentation of cauda equina?
LMN signs
- Reduced lower limb sensation (often bilateral)
- Hyporeflexia
- Bladder or bowel dysfunction:
a. Perianal (saddle) numbness
b. Loss of anal tone
c. Urinary retention
- Lower limb motor weakness
- Severe back pain
- Impotence
Investigations for cauda equina?
PR examination
Post-void bladder scan
Lumbar-sacral spine MRI
Management of cauda equina syndrome?
Management
- Surgical decompression within 48 hours
- Radiotherapy and/or chemotherapy
- In patients where malignancy is demonstrated on MRI, or in patients where clinical suspicion is high, administration of dexamethasone 16 mg daily in divided doses (with PPI cover) is indicated.
What are common causes of Nausea and Vomitting in pts with cancer?
surgical sieve e.g. infection
AR the mechanisms / pathophysiology of nausea and vomitting
Recap: which anti-emetics work on which recpetors to combat nausea and vomitting?
Chemical cause of N&V:
1. what would be clinical features?
2. What is best antiemetic?
Gastric stasis is cause of N&V
1. clinical features?
2. treatment?
Bowel obstruction is the cause of N&V
1. clincial features
2. treatment?
Raised ICP is cause of N&V
1. clinical features
2. treatment
Psychological factors causing N&V
1. features
2. treatment
Post op / RT causes of N&V
1. features
2. treatment
Constipation causes N&V
1. clincial features
2. treatment
How many cancer pts get N&V?
Up to 75% of all cancer patients will experience chemotherapy related emesis
What are some increased risks for N&V when have cancer?
- Increased risk associated with specific chemo
agents
female gender
age <50 years
past Hx
of N&V (pregnancy, prior chemotherapy use,
motion sickness)
features of N+V caused by chemotherapy
persistent, often severe nausea, unrelieved by vomiting, aggratated by sight/smell of food
Management after sickness inducing chemotherapy
- Metoclopramide
- Dexamethasone
- Ondansetron
Non-pharmacological management:
* Advice and realistic aims
* Smell
* Taste - small appropriate meals
* Hypnosis?
* Acupuncture?
timings wise how can chemotherapy induced nausea and vomitting present?
Acute, delayed, anticipatory
management of route and regime in a patient with nausea and vomtiing
Route and regime:
* Oral absorption likely to be poor
* Consider SC route for at least 24 hours
* Regular anti-emetic
* Consider alternative if not improving
* Control of symptoms using one antiemetic is possible in ~60% of patients
* 1/3 require concurrent use of a second antiemetic
* Combine anti-emetics with different mechanisms of action
* Consider switch to oral if improving
* Cause resolves…?stop
which symptoms except pain may be need to be managed in a cancer pt?
- Nausea and vomiting
- Intractable breathlessness
- Constipation
- Psychological distress, depression and anxiety
- Confusion and delirium
Clinical features of constipation?
What can it lead to?
causes of constipation?
Give examples of laxatives, their class, and their mechanism of action
- Laxido and Movicol popular in oncology
- Rarely use lactulose because poorly tolerated due to sweetness, except encephalopathy
Which cancer pts get malignant bowel obstruction
- Effects up to 15% of cancer patients
- Ovarian (20-50%)
- Colon (10-29%)
Pathophysiology of malignant bowel osbtruction?
- Mechanical (tumour within gut lumen or outside bowel wall)
- Functional: (infiltration of myenteric plexus +/or gut musculature)
- Combination of mechanical + functional
- Gradual onset common
How to treat malignant bowel obstruction
How to treat inoperable bowel obstruction?
If inoperable malignant bowel obstruction is NOT resolving despite initial interventions. What can you do next?
SUMMARY SLIDE : N&V causes and treatment!
compare cyclizine and metoclopramide
The oppose each in other !
- metoclopramide -> prokinetic
- good for nausea and vomiting caused by chemo/ cancer
- Cyclizine -> antikinetic (opposite affect to meto)
- good for bowel obstruction
presentation of breathlessness
- Patient-centred symptom
- Cannot be inferred from physical examination or investigation- must ask about it
treatable causes of breathlessness i.e. give examples and how they are treated
Prevalenceof breathlessness?
Pathophysiology of breathlessness
- neurophysiology of breathlessness is related to but distinct from the control of the respiratory system
- Breathlessness is a MISMATCH between the pts percieved need to breathe (respiratory drive) and their ability to do so (physiological capacity)
Non drug management of intractable breathlessness?
- Aim to reduce the perception
- Patients can quickly detect lack of HCP confidence- calm, positive, logical approach needed
- Position patient using gravity and not hinder weak diaphragm/ chest wall muscles
- Air flow across face: fan or open a window
- Trial of oxygen (if hypoxic)
- Non-drug approaches if feasible
Intractable breathlessness : drug management
what is intractable breathlessness?
sustained severe breathlessness in patients who have not obtained relief from conventional treatment.
Causes of hypercalcaemia?
capsule
Most common:
* primary hyperparathyroidism i.e. parathyroid adenoma / MENI/II
Hypercalcaemia of malignancy
Sarcoidosis
thryrotoxicosis
thiazide diuretic
Signs and symptoms of hypercalacaemia
capsule onoclogy
Abdo pain
nausea and vomiting
constipation
polyuria
polydipsia
depression
confusion
renal stones
renal failure
Which cancers commonly causes bony tumour deposits?
capsule oncology
breast
prostate
lung
thyroid
renial
myeloma
melanoma
