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Cancer care (Y4) > 12- Acute presentations in cancer (secondary to cancer) > Flashcards

12- Acute presentations in cancer (secondary to cancer) Flashcards

1
Q

Bowel obstruction
Background

A
  • Complication of advanced cancer
  • Can happen when
    o Cancer in abdominal area
     Ovarian(40%)
     Bowel
     Stomach cancer
    o Metastasis
    o Cancer grows into nerve supply of bowel and stops muscles working
    o Adhesions due to past abdominal surgery
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2
Q

Risk factors for bowel obstruction secondary to cancer

A
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3
Q

Presentation of bowel obstruction

A
  • Stomach pain- colicky
  • Constipation
  • Vomiting
    o Occurs early in upper GI obstruction and later in lower GI
  • Abdominal distension
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4
Q

Investigations for bowel obstruction

A
  • Abdominal X ray
    o Central- upper
    o Peripheral- lower
  • CT scan
  • Barium enema
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5
Q

management of bowel obstruction in cancer

A

Will depend on cause and stage of cancers
Supportive
- NG decompression/ venting gastrostomy (PEG)
- IV fluids to prevent rehydration

Medication
- Buscipan- stop muscle spasms and reduce pain
- Strong painkillers
- IV antibiotics
- Antiemetics
- Octreotide
o Reduces fluid that building up in GI tract
- Steroids to reduce inflammation in bowel

Surgery
Tends to be palliative to relieve pain
- Resection of damaged bowel-> stoma
- Stent insertion

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6
Q

Superior vena cava obstruction
Background

A
  • Primary lung cancer e.g. Pancoast tumour
    o Small
    o Squamous
  • Lymphoma
  • Metastasis
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7
Q

Superior vena cava obstruction

Pathophysiology

A
  • Tumour presses on SVC
  • Less blood draining from veins in the brain into the heart
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8
Q

presentation of SVCO

A

Presentation
- Tachycardia, tachypnoea, hypotension
- Swollen, red face
- Neck and shoulder swollen
- Jugular venous distension
- Pemberton sign

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9
Q

Pemberton sign

A
  • Ask patient to raise both arms above head
  • Normal: nothing
  • SVC syndrome: facial and neck swelling, cough, SoB, cyanosis
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10
Q

Investigation for SVCO

A
  • CT scan with contrast
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11
Q

Complications of SVCO

A
  • Tracheal obstruction
  • Resp distress
  • Hypotension and tachycardia
  • Cyanosis
  • Retinal haemorrhage
  • Stroke
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12
Q

Management of SVCO

A

Dexamethasone

  • Mild
    o Head elevation and diuretics
    o Endovenous stents
  • Palliative care
    o Cryotherapy
    o Diathermy
    o Bronchial stents for central airway
    o Endobronchial radiotherapy
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13
Q

Hypercalcaemia
Background

A

Hypercalcaemia is defined as correct calcium >2.65mmol/L.

  • Normal range 2.2-2.51 mmol/l
  • Can be free or bound to albumin
    o Adjusted for how much albumin in blood
    o If low albumin – free albumin will be making up a higher amount of calcium
  • Common complication
  • Occurs most often in disseminated disease- poor prognosis
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14
Q

pathophysiology of hypercalcaemia related to malignancy

A
  • Humoral cause (80%)
  • Bone invasion
  • Tymour calcitriol release
  • immunotherapies and hormonal therapy
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15
Q

humoral cause of hypercalcaemia

A
  • Chemical agents released by tumour disrupt normal calcium homeostasis e.g. PTH-related protein released by certain cancers
  • E.g. paraneoplastic feature of lung cancer – SCC
  • Causes increased release of calcium from bone and increase uptake from kidneys
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16
Q

bone invasion and hypercalcaemia

A

Osteolytic metastases with local release of cytokines -> increased bone reportion and therefore calcium release from bone into blood

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17
Q

Risk factors for hypercalcaemia

A
  • Breast cancer
  • SCC
  • Renal
  • Myeloma
  • Lymphoma
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18
Q

Presentation of hypercalcaemia

A

Bones, moans, groans, stones, psychiatric overtones
- Nausea
- Anorexia
- Thirst
- Constipation
- Kidney stones
- Confusion
- Polydipsia and polyuria
- Fatigue and weakness
- Bone bane
- Neurological
- Cardiac

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19
Q

hypercalcaemia and neuro effect

A

o Seizures
o Poor coordination
o Change in personality

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20
Q

hypercalcaemia and cardiac effect

A

o Bradycardia
o HTN
o Shortened QT interval

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21
Q

calcium homeostasis

A

1) Reduction in calcium detected by the PTH gland
2) Increase PTH secretion
3) Increase PTH in plasma
- In the bone- increases reabsorption (from bone into blood) of calcium and phosphate – increases plasma Ca2+

  • In the kidney
    o Calcium reabsorption in nephron increases
    o Reduced excretion of calcium in urine
    o Reduction in reabsorption of phosphate (PCT)
    o Increase excretion of phosphate
    o Reduce plasma phosphate, therefore higher calcium in plasma (inversely proportional)
  • Vitamin D
    o PTH causes increased 1,25 dihydroxycholecalciferol formation (active vitamin D ) in the kidney
    o Enhances absorption of calcium from intestine
    o Increase calcium absorption
    o Increase plasma calcium

4) Restore plasma calcium to normal – negative feedback to PTH gland

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22
Q

calcitonin

A

a peptide released from the thyroid- has an opposite effect to PTH
- when PT detects high calcium- calcitonin released

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23
Q

investigations for hypercalcaemia

A

Assessment of the hypercalcaemic patient should include:

  • 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
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24
Q

ECG and hypercalcaemia

A

o Osborn wave
o ST segment elevation
o Biphasic T waves
o Prominent U waves

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25
Q

management of hypercalcaemia

A

Management of acute hypercalcaemia is focused around treating the immediate complications and reducing calcium release into the blood:

1) Aggressive IV fluids (corrects dehydration, protects the kidneys and increases calcium excretion)
- normal saline
2) Bisphosphonates e.g. Zolendronate (inhibits osteoclast activity reducing calcium release)
- IV pamidronate or zolendronic acis
- Can cause renal failurew so must be properly rehydrated first
- Denosumab for refractory hypercalcaemia
3) Further management to prevent recurrence (depending on the cause):
* Chemotherapy (malignancy)
* Surgical resection (malignancy)
* Radiotherapy (malignancy)
* Steroids (sarcoidosis)
* Calcitonin
* Furosemide

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26
Q

Prognosis of hypercalcaemia and malignancy

A
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27
Q

Why bisphosphonates with hypercalcaemia

A
  • Ca2+ and PO4 3- concentrations are inversely proportional
  • High calcium and low phosphate or low calcium and high phosphate
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28
Q

VTE
Background

A
  • 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
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29
Q

Pathophysiology of VTE and malignancy

A
  • Hypercoagulable state induced by specific prothrombotic properties of cancer cells that activate blood clotting
  • Activation of:
    o Platelets
    o Leukocytes
    o Endothelial cells
  • Also endothelium activation by anti-cancer drugs
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30
Q

Risk factors for VTE

A
  • Cancers at highest risk
    o Pancreatic
    o Gastric
    o Lung cancers
  • Patient risk factors
    o CVD
    o Smoking
    o Obesity
    o COCP/HRT
  • Cancer treatments
    o Cisplatin
    o Tamoxifen
  • Being less active
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31
Q

Presentation of VTE

A
  • DVT
    o Redness
    o Tenderness
    o Swelling
    o Pitting oedema
    o Collateral superficial veins
  • PE
    o SoB
    o Chest pain
    o Cough
    o Tachycardia
    o Cyanosis
    o Dizziness and fainting
    o sweating
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32
Q

investigations for VTE

A
  • D-dimer raised in cancer so not used as a predictor
  • DVT- US
  • PE- CTPA
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33
Q

Management of VTE

A

DOAC +- LMWH, warfarin, LMWH alone
- DOACS
o Apixaban
o Dabigatran
o Edoxaban
o Rivaroxaban
- LMWH
o Dalteparin
o Enoxaparin

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34
Q

Reducing risk of blood clots whilst in hospital

A
  • Anticoagulants
  • Antiembolic stockings
  • Compression devices
  • Keeping moving
  • Stopping COCB or HRT
  • Keeping hydrated
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35
Q

GI bleeding
Background

A
  • Common in patients with solid cancers and also those with bone cancers due to thrombocytopenia
  • Problem in advanced cancers mostly
  • Divided into
    o Upper and lower
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36
Q

Causes of bleeding secondary to cancers

A
  • 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
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37
Q

Upper GI bleed

A
  • Gastric ulcer (splenic artery erosion)
  • Duodenal ulcer
  • Oesophageal varices
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38
Q

Presentation of upper GI bleed

A
  • Haematemesis
    o ‘Vomiting blood’ – caused by bleeding from the upper portion of the GI tract. Wide range of causes depending on the site of blood loss and the tissue bleeding.
    o Coffee ground vomiting- digested blood
  • Melaena – tar like, black greasy and offensive stools caused by digested blood- oxidised
  • Haemodynamic instability
  • Epigastric pain
  • Jaundice for ascites in decompensated lived disease ->pneumoperitoneum
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39
Q

Scoring systems for Upper GI bleed

A

Glasgow-Blatchford score and Rockall

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40
Q

Glasgow-Blatchford score

A

Scoring system in suspected upper GI bleed on their initial presentation. It scores patient based on their clinical presentation. It establishes their risk of having an upper GI bleed to help you make a plan (for example whether to discharge them or not).
Using an online calculator is the easiest way to calculate the score. A score > 0 indicates high risk for an upper GI bleed. It takes into account various features indicating an upper GI bleed:
* Drop in Hb
* Rise in urea
o Blood in GI tract gets broken down and urea is a by-product absorbed in the intestine
* Blood pressure
* Heart rate
* Melaena
* Syncope

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41
Q

Rockall

A
  • Used in pts that have had an endoscopy to calc their risk of rebleeding and overall mortility .
  • Online calculator
    o Age
    o Features of shock (e.g. tachycardia or hypotension)
    o Co-morbidities
    o Cause of bleeding (e.g. Mallory-Weiss tear or malignancy)
    o Endoscopic stigmata of recent haemorrhage such as clots or visible bleeding vessels
42
Q

rockall vs glasgow-blatchford score

A

Glasgow- blatchford
- establishes risk of having an upper GI bleed in order to make a plan e.g. discharge them or not

Rockall
- calc risk of rebleeding and overall mortality

43
Q

management of upper GI bleed

A
  • ABATED
    o A – ABCDE approach to immediate resuscitation
    o B – Bloods
    o A – Access (ideally 2 large bore cannula)
    o T – Transfuse (group and save, if varices 4units blood cross-matched))
    o E – Endoscopy (arrange urgent endoscopy within 24 hours)
    o D – Drugs (stop anticoagulants and NSAIDs)
  • Bloods
    o Haemoglobin (FBC)
    o Urea (U&Es)
    o Coagulation (INR, FBC for platelets)
    o Liver disease (LFTs)
    o 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

44
Q

Ulcers
Pathophysiology

A

Erosion of blood vessels supplying upper GI tract
- Lesser curve of stomach (20%)
- Posterior duodenum (40%)
o Gastroduodenal artery most common

45
Q

Risk factor for ulcers

A

o Ulcer disease/ H.pylori positive
o NSAID
o Steroids

46
Q

investigation for ulcers

A

Investigations
o Erect CXR if suspect peptic ulceration

47
Q

Management of ulcers

A

o A to E
o Injection of adrenaline and cauterisation of bleeding
o High dose IV PPI therapy (e.g. IV 40mg of omeprazole) to reduce acid secretion
o +/- H.Pylori eradication therapy if necessary

48
Q

Oesophagitis

A

Inflammation of intraluminal epithelial layer of the oesophagus
Inflammation of intraluminal epithelial layer of the oesophagus
Causes
- GORD
- Infections e..g candia albicans
- Medication (bisphosphonates)
- Radiotherapy
- Ingestion of toxic substance
- Crohns disease

  • GORD
  • Infections e..g candia albicans
  • Medication (bisphosphonates)
  • Radiotherapy
  • Ingestion of toxic substance
  • Crohns disease
49
Q

Oesophageal varices

Causes

A
  • Dilation of portosystemic venous anastomoses in oesophagus
  • Thin, swollen and dilated- prone to rupture
  • Most common
50
Q

Risk factors for oesophageal varices

A
  • Alcoholic liver disease
  • liver cancer or metastatic liver cancer
51
Q

Management of oesophageal varices

A
  • Same as general upper GI bleed
  • Additional steps: management should be swift and performed at the same time as active resuscitation, including the use of blood products and prophylactic antibiotics
    o Endoscopic banding is the most definitive method of management* however can be technically difficult
    o Vasopressors (e.g. terlipressin) should also be started, acting to reduce splanchnic blood flow and hence reduce bleeding
    o Long term management warrants repeated banding of the varices and long-term beta-blocker therapy
    o Prophylactic broad spectrum antibiotics
52
Q

Lower GI bleed

Main symptom:

A

rectal bleeding (haemtochezia)
- passage of fresh blood per rectum

53
Q

causes of lower gI bleed

A

Causes
- Diverticular disease
- Ischaemic or infective colitis
- Haemorrhoids
- Malignancy
- IBD
- Radiation proctitis

54
Q

History taking for lower GI bleed

A
  • 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
55
Q

Examination for lower GI bleed

A
  • The abdomen for any localised tenderness or masses palpable.
  • A PR examination is essential for every patient presenting with haematochezia, allowing assessment for any rectal masses and ongoing presence of blood
56
Q

Investigation for lower GI bleed

A
  • Bloods- FBC, U&Es, LFT, clotting
    o Acute bleed may not show reduced Hb levels, ongoing bleeding will
  • Group and save
  • Stool culture
    - Haemodynamically unstable
    o Stabilised before undergoing urgent CT angiogram
    -> Can identify source of bleeding
    - Haemodynamically stable
    o Flexible sigmoidoscopy (exclude left colonic pathology)- can be outpatient
  • If PR bleeding back no abnormality found on colonoscopy- look for upper GI bleed- OGD
57
Q

conservative management of lower GI bleed

A

Young, haemodynamically stable patients with low risk score can be discharged and investigated as outpatient

58
Q

management of unstable lower GI bleed

A

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
o Injection (diluted adrenaline)
o Contact and non-contact thermal devices (bipolar electrocoagulation)
o 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

59
Q

ascites background

A
  • Pathological accumulation of ascitic fluid in the peritoneal cavity
  • Peritoneum makes up ascitic fluid -> if it builds up -> ascites

Causes
* Portal hypertensions (cirrhosis, heart failure, liver cancer)
* Non-portal hypertension
–> Hypoalbinemia, malignant, infection

60
Q

Pathophysiology of ascites

A

- Cancer of the liver
o Portal hypertension forces fluid out of nearby blood vessels
o Damage to the liver reducing albumin production -> reduced hydrostatic pressure

- Metastasis to the peritoneum
o Makes it leaky- malignant ascites

61
Q

presentation of ascites

A

Presentation
- Swelling of the abdomen
- Tightness
- Feeling full when eating
- Nausea
- SoB
- If infected
o Pain
o Fever

62
Q

investigations for ascites

A
  • US
  • Needle aspiration- paracentesis
    o WBC, blood, cancer cells, bacteria
    o If cancer cells found- malignant
  • Examination- shifting dullness
63
Q

Management of ascites

A

Depends on cause, severity of symptoms, extent of spread and suitability for anticancer treatment
- If liver damage the cause
o Diuretic e.g. spironolactone
o Reduce salt

  • If very symptomatic
    o Paracentesis
    o Provides immediate relief
    o Fluid can return and procedure repeated
    o If recurring- indwelling catheter
  • Treating the cancer
    o chemotherapy
64
Q

Pleural effusion
Background

A
  • Pathological accumulation of pleural fluid in the pleural cavity
65
Q

pathophysiology of pleural effusion

A
  • Lung infections
  • Heart failure
  • Metastatic cancer
    o Lung cancer
    o Breast cancer
    o Ovarian cancer
    o Lymphomas
  • Primary cancers
    o Mesothelioma (cancer of the pleura)

In normal pleural cavity there is tightly controlled production and absorption of pleural fluid.

66
Q

Presentation of pleural effusion

A
  • Breathlessness
  • Cough
  • Chest pain
  • Examination
    o Stony dullness
    o Trachea pushed away from effusion
67
Q

Investigations for pleural effusion

A
  • Chest X-ray
  • Test fluid for: WBC, cancer, 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
o Biochemistry (protein, pH, LDH
o Cytology
o Microbiology
- If no tracheal deviation then pathology may be a mixture of atelectasis and effusion (pull + push = no deviation)
- Will need to do a bedside US to determine if fluid or collapse

68
Q

Management of pleural effusion

A

Never inset a chest drain unless diagnosis is well established e.g. known metastatic lung cancer, otherwise draining fluid may hinder opportunity to obtain pleural biopsies
Chest drain
- Complications: blocked drain, infected drain, pneumothorax, recurrence
Recurrent
- Catheter insertion
- Pleurodesis
–> Fusion of 2 pleural layers

69
Q

transudate or exudate

A
70
Q

Causes of Transudate effusions (pleural protein <30 g/L)

A

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

71
Q

Causes of Exudate effusions (pleural protein >30 g/L)

A

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

72
Q

Raised intracranial pressure
Background

A

Principle cause of RICP in cancer patients is
- Space-occupying tumour
- Obstructive hydrocephalus

73
Q

Raised intracranial pressure
Background

A

Principle cause of RICP in cancer patients is
- Space-occupying tumour
- Obstructive hydrocephalus

74
Q

Presentation of SoL

A
  • N and V
  • Dizziness
  • Changes in eyesight
  • Behaviour changes
  • Neurological problems
    o Eyesight
    o Weakness and numbness
    o Coordination problems
    o Arthralgia
    o Reduced consciousness
  • Worse on cough
  • Worse on leading forwards
  • Coning symptoms- emergency
    o Bradycardia
    o High blood pressure
    o Abnormal breathing
75
Q

Investigations of RICP

A
  • CT scan +- MRI with and without contrast
  • Fundoscopy
    o Papilledema
    o Loss of retinal venous pulsation
  • Lumbar puncture-> to determine CSF pressure and look for cancer cells
76
Q

Management of RICP

A
  • Dexamethasone to shrink tumour
  • Antibiotics if infective cause
  • Cancer treatment if SoL
    o Debulking surgery
    o Radiation therapy
    o Intrathecal chemotherapy- given via lumbar puncture
  • Surgery
    o Cerebral shunts placed tp drain CSF and lower ICP
    o CSF is drained from brain to the abdomen
77
Q

status epilepticus background

A
  • Risk of epileptic seizures increase in cancer patients due to
    o Brain metastases and
    o Primary brain tumour
  • Status epilepticus is define as a seizure lasting longer than 5 minutes or more than 1 seizure in 5 mins
78
Q

Risk factors for status epilepticus

A
  • Slow growing , low grade tumour
  • Tumour is in one of the lobes of the cerebrum or meninges
79
Q

Pathophysiology of status epilepticus

A
  • Due to abnormal development of cells around the tumour that have developed abnormally
  • May be due to imbalance of chemicals in the brain caused by tumour
  • Leads to altered electrical activity in the brain -> epilepsy
80
Q

managemetn of frequent seizures

A

Management
Anti-epileptics
Frequently used anti-convulsants include:
* levetiracetam (Keppra®)
* sodium valproate (Epilim®)
* lamotrigine (Lamictal®)
* clobazam
* carbamazepine (Tegretol®)
* topiramate
* phenytoin (Epanutin®).
Surgery- neurosurgery

81
Q

status epilepticus emergency management

A

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

82
Q

Metastatic spinal cord compression
Background

A
  • 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
83
Q

Risk factors for metastatic cord compression

A
  • It is more common in patients with lung, breast and prostate cancer
84
Q

pathophysiology of NSCC

A
  • Occurs when dural sac and its contents are compressed at the level of the cord or cauda equina
  • Causes
    o Collapse of vertebral body due to bony mets causing brittle bones
    o Metastasis in the epidural space (paraspinal area)
    –> Especially lymphoma
85
Q

Damage to cord stages

A

1) Reversible initial stages
- Initially oedema
- Venous congestion
- Demyelination

2) Prolonged compression
- Vascular injury
- Cord necrosis
- Permanent damage

86
Q

presentation of MSCC

A

Back pain
- 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

Motor symptoms (upper motor neuronee signs)
- Affects >75%,
- Reduced power, difficulty standing, walking, climbing stairs, often symmetrical
- (high cervical scc causes poor truncal balance)

Sensory loss
- Affects >50%, but may be unaware until examined

Sphincter dysfunction
- Urinary hesitancy, frequency, then urinary retention with overflow, faecal incontinence
- Diminishing performance status/generally unwell

87
Q

examination of someone with MSCC

A
  • Acute onset -> Flaccid paralysis
  • Progressive (UMN)
    o Spasticity (increased tone, clonus, hyperreflexia in limbs below level of MSCC)
    o Plantar reflexes up-going - Babinski(not cauda equina- LMN)
    o Palpable bladder (urinary retention)
    o Sensory loss with well define dermatomal levels
  • Cauda equina
88
Q

Location of MSCC

A
  • Thoracic commonest site
  • 30-50% >1 areas involves
  • Below L2 vertebra= cauda equina(compression of peripheral nerve and not spinal cord)
89
Q

investigation for MSCC

A
  • MRI of the whole spine
  • Routine. Blood tests
  • If high chance of surgery- Group and save and clotting screen
90
Q

referral for MSCC

A

Referral
- Pain suggestive of spinal mets – MRI within 1 weeks
- Signs MSCC, MRI within 24 hours

91
Q

UMN vs LMN signs

A

UMN
- Spinal cord compression
o Hypertonia
o Hyperreflexia
o Babinskis sign
o clonus

LMN
- Cauda equina
- Peripheral nerve compression

92
Q

inittial manaegment of MSCC

A

Initial management
- Admit and treat within 24 hours of diagnosis
- Bed rest with log-rolling
- Dexamethasone 16mg + PPI
- Adequate analgesia
If >48hrs no motor function -> supportive care
- Analgesia
- Laxative
- Care of pressure areas
- Bladder
- Care
- Mnitor BMs
- VTE prophylaxis
- Physiotherapy
OT

93
Q

surgery for MSCC

A

Surgery
- First line treatment- Balloon kyphoplasty
- Best suited
o MM
o Lymphoma
o Breast
o Prostate
o Renal
- Ideal candidates
o Good motor function at presentation
o Good performance status
o Limited comorbidity
o Single level spinal disease
o Absence of visceral mets
o Long interval from primary diagnosis
o Helpful for biopsy/ stabilisation
- Aim
o Relive compression
o Remove tumours
o Stabilise spine
o Preserve greater degree of mobility

94
Q

radiation and MSCC

A

Radiotherapy
- Majority receive this (due to extensive disease and poor performance status when MSCC occurs)
- Delivered within 24 hours
- MOA
o Targets abnormal area plus 1-2 vertebra either side
- Aim
o Relieve compression of the spine and nerve roots by causing cell death in the rapidly dividing tumour tissue
o Relives pain and stabilises neurological deficict
- Life expectancy often measured in months

95
Q

chemotherapy and MSCC

A

Urgent chemotherapy
- May be considered if very sensitive tumours e.g. lymphoma /SCLC

96
Q

cauda equina syndrome background

A
  • Surgical emergency
  • Caused by compression of the spinal cord
    o Below L2
    o Peripheral nerves (LMN), containing motor and sensory fibres
  • High level of suspicion and rapid intervention required
97
Q

pathophysiology of cauda equina syndrome

A

Causes
- Disc herniation
- Trauma
- Neoplasm
o Primary or metastatic
o Most common cancers that spread to spinal vertebrae: thyroid, breast, lung, renal and prostate)
- Infection
- Chronic spinal inflammation
- Iatrogenic

98
Q

presentation of cauda equina

A

Lower motor neurone signs
- Reduced lower limb sensation (often bilateral)
- Hyporeflexia
- Bladder or bowel dysfunction
o Perianal (saddle) numbness
o Loss of anal tone
o Urinary retention
- Lower limb motor weakness
- Severe back pain
- Impotence

99
Q

investigations for cauda equina

A
  • PR examination
  • Post-void bladder scan
  • Lumbar-sacral spine MRI
100
Q

management of cauda equina syndrome

A

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.

Cancer care (Y4) (30 decks)

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