Cancer-related emergencies (Year 5 OSCE) Flashcards
Neutropenic Sepsis
- Definition
- Causes
- Risk factors
- Presentation and examination
- Investigations
DEFINITION
- Neutrophil count of 0.5 × 10^9 per litre or lower, and either
- Temperature ≥ 38°C or
- Signs or symptoms of significant sepsis
CAUSES:
- Recent chemotherapy within 7 – 10 days
- Bone marrow infiltration (malignant or not)
- Extensive radiotherapy
- Bone marrow failure secondary to non-malignant disease (e.g. aplastic anaemia)
- Hypersplenism
- Megaloblastic anaemia
- Drug-induced (e.g. clozapine)
RISK FACTORS:
- Age > 60
- Advanced malignancy
- Previous neutropenic sepsis
- Mucositis
- Significant co-morbidities
- Indwelling central venous catheters
- Corticosteroids
- Prolonged hospital admission
PRESENTATION:
- Fatigue
- Feeling warm or cold
- Rigours or shaking
- Feeling sweaty or clammy
- Palpitations
- Dizziness
- Subjective confusion or disorientation
- Ask about PMH of chemotherapy, especially within past 7 – 10 days
SPECIFIC PRESENTATIONS:
- Chest source: shortness of breath, cough, chest pain, sore throat.
- Urine source: dysuria, increased frequency, urgency or any other lower urinary tract symptoms.
- Skin source: rashes, blisters, pain.
- Gastrointestinal source: diarrhoea, nausea, vomiting, rectal bleeding, abdominal pain, sore mouth (due to mucositis).
- Indwelling line source: pain around the line or rigours after use of the line
ALSO ASK IN HISTORY:
- Past medical history (e.g. details of cancer diagnosis including previous treatments)
- Chemotherapy history (e.g. type of chemotherapy, date of the most recent cycle)
- Drug history (e.g. steroids, antibiotic prophylaxis, granulocyte-colony stimulating factor use and details of any allergies)
- Recent procedures which may predispose to infection (e.g. placement of an indwelling vascular access device)
- Previous episodes of pyrexia or neutropenic sepsis (to guide the identification of a source or causative organism)
O/E:
- Haemodynamic instability (e.g. hypotension, tachycardia, tachypnoea, hypoxia)
- Fever
- Reduced urine output
- Altered conscious level or confusion
- Mottled/ashen appearance
SPECIFIC SIGNS O/E:
- Chest source: increased work of breathing, crepitations, dullness to percussion, reduced air entry.
- Urine source: suprapubic or flank pain, cloudy urine in catheter bag (if applicable).
- Skin source: rashes, blistering, tenderness.
- Gastrointestinal source: abdominal tenderness, dehydration (if reporting vomiting or diarrhoea), evidence of oral mucositis, jaundice.
- Indwelling line source: surrounding erythema, tenderness on palpation, pain or rigors on flushing.
INVESTIGATIONS:
a) Bedside
- Urinalysis: for UTI
- BM to exclude hypoglycaemia.
- ECG for arrhythmia
- Sputum samples if respiratory source suspected
b) Bloods
- Baseline blood tests (FBC, U&E, coagulation, CRP, LFTs): WCC may be low or raised, CRP elevated
- Serum lactate: raised in advanced malignancy
- Group and save: for blood transfusion.
- Blood cultures: at least two sets from a peripheral vein plus a set from an indwelling line if present to look for a causative organism.
- ABGs: to identify respiratory failure
- Microbiological cultures: wounds, urine, stool, sputum, and line tip (if indwelling line infection suspected)
- Viral respiratory swab: if viral respiratory infection suspected
c) Imaging
- Chest X-ray: to look for pneumonia.
- High-resolution chest CT: if fungal pneumonia is suspected.
- Abdominal USS or CT abdomen: if biliary or abdominal infection suspected.
Tumour Lysis Syndrome
- Definition
- Pathophysiology
- Risk factors
- Presentation and examination
- Investigations
- Diagnostic criteria
DEFINITION:
- Tumour lysis syndrome (TLS) results from metabolic disturbances arising from the breakdown of malignant cells following the initiation of treatment for malignancy
PATHOPHYSIOLOGY:
- Cytotoxic-mediated lysis of tumour cells lead to the release of intracellular components, such as K+, phosphates and nucleic acids, into the systemic circulation
- Consequences include hyperkalaemia, hyperphosphataemia and hyperuricaemia
- Hypocalcaemia develops secondary to hyperphosphataemia with the precipitation of calcium in soft tissues.
- Hyperuricaemia occurs due to the metabolism of nucleic acids. Purines within these nucleic acids are metabolised initially to hypoxanthine, which is then metabolised to xanthine and uric acid
RISK FACTORS:
- Burkitt’s leukaemia and certain Burkitt’s lymphoma
- ALL with certain WBC and LDH criteria
- AML with high WBC counts
- Certain NHLs with high LDH and bulky disease (e.g. diffuse large B-cell, peripheral T-cell, mantle cell)
[IE: TLS is more likely with haematological malignancy]
PRESENTATION:
(Onset 3-7 days following the initiation of treatment)
- Lethargy
- N & V
- Diarrhoea
- Anorexia
- Muscle cramps
- Syncope
- Pruritus
- Arthritis
- Paraesthesia
- Palpitations (ie: arrhythmias)
- Seizure
- Sudden death
[NB: timing is crucial in differentiating TLS from NS: TLS will present earlier following chemotherapy while NS presents later]
O/E:
- Fluid overload
- Signs of hypocalcaemia: tetany, trousseau’s sign (carpopedal spasms following inflation of the blood pressure cuff) and Chvostek’s sign (tapping over the course of the facial nerve induces abnormal twitching of the facial muscles)
- Bronchospasm (wheezing)
INVESTIGATIONS:
a) Bedside
- ECG for signs of hyperkalaemia such as tall-tented T waves, P wave flattening, PR interval prologation, QRS widening, sine waves (late sign) and signs of hypocalcaemia such as QTc prolongation
- Urine sample for microscopy may reveal urate crystals
b) Bloods
- Renal function, U&Es to reveal electrolyte imbalances (esp potassium and phosphate)
- Serum urate raised
- Serum calcium low
- Serum creatinine raised
- LDH rasied
[NB: bloods to assess the severity of TLS; should be monitored every 4-6 hours if high risk]
DIAGNOSTIC CRITERIA FOR TLS:
“Cairo-Bishop Definition”
a) Laboratory diagnosis
- Urate > 476 mcmol/L or 25% increase
- Potassium > 6 mmol/L or 25% increase
- Phosphate > 1.45 mmol/L or 25% increase
- Calcium < 1.75 mmol/L or 25% decrease
[any 2 or more of the above within 3 days or after 7 days from beginning treatment]
b) Clinical diagnosis
- Any patient who meets criteria for laboratory diagnosis, AND has one or more of the following:
- Serum creatinine > 1.5x normal
- Arrhythmia or sudden death
- Seizure
Tumour Lysis Syndrome: principles of management and prophylaxis?
MANAGEMENT:
a) Hyperphosphataemia
- Hydration (oral or IV)
- Dietary restriction of phosphate
- Phosphate binders
b) Hyperkalaemia
- IV calcium gluconate to stabilise myocardium
- Insulin with dextrose to increase cellular uptake of K+
- NEB salbutamol
- Cardiac monitoring if K+ > 6 mmol/L or > 25% increase from baseline
c) Hypocalcaemia
- If asymptomatic, do not treat as this can increase calcium phosphate deposits in the kidneys causing AKI
- Cardiac monitoring for calcium < 1.75 mmol/L or > 25% decrease from baseline
- Only consider IV replacement if symptomatic
d) Renal failure
- Hydration (oral or IV)
- Consider haemofiltration if refractory hyperkalaemia, fluid overload, hyperphosphataemia-induced symptomatic hypocalcaemia, or high calcium-phosphae product
PROPHYLAXIS:
- The prevention of TLS requires the risk stratification of patients prior to the initiation of cytotoxic therapy.
- Patients are grouped into low, intermediate and high risk. Prophylaxis may take the form of oral hydration, intravenous hydration, allopurinol and rasburicase.
- All patients to be monitored for the development of any clinical or biochemical evidence of TLS
- LOW RISK OF TLS:
- Oral hydration, no need for hypouricaemic agents - INTERMEDIATE RISK OF TLS:
- IV hydration, and
- Allopurinol 300 mg daily for up to 7 days following the initiation of cytotoxic therapy; works by inhibiting xanthine oxidase (XO), which converts hypoxanthine to uric acid - HIGH RISK OF TLS:
- IV hydration, and
- Rasburicase stat dose of 3mg; it is a recombinant urate oxidase enzyme which breaks down urate into soluble metabolites
Neutropenic Sepsis:
- Basic principles of management
- Antibiotic choices
BASIC PRINCIPLES OF MANAGEMENT:
- Empirical antibiotics stat within one hour of admission ASAP
- Sepsis 6 bundle
- Call senior help
- Urgent bloods (esp: FBC)
[NB: do NOT delay to investigate]
ANTIBIOTIC CHOICES:
- 1st line: IV piperacillin with tazobactam (tazocin) +/- gentamicin
- 2nd line: (e.g. penicillin allergy) IV meropenem
- 3rd line: additional anti-microbial cover (e.g. teicoplanin) for gram-positive organisms for patients with indwelling central venous catheters.
- Consider anti-fungal treatment if fever persists beyond 4 – 6 days
- Consider G-CSF as prophylaxis or treatment; works by stimulating bone marrow to produce neutrophils
GCSF PRINCIPLES OF TREATMENT:
- Recombinant G-CSF may be used for both prophylaxis and treatment of neutropenia to reduce the risk of neutropenic sepsis.
- G-CSF works by stimulating the bone marrow to produce neutrophils and may form part of specific chemotherapy regimens. An example of a G-CSF drug is filgrastim
Malignant Spinal Cord Compression:
- Causes and aetiologies
- Locations
- Presentation and examination
- Investigations
CAUSES AND AETIOLOGIES:
- Primary malignancy: primary bone tumours or CNS malignancies
- Secondary malignancy: lungs, kidney, breasts, prostate, thyroid, pathological fracture due to cancer, multiple myeloma
- Other non-malignant causes: trauma, disc prolapse, haematoma, epidural abscesses
LOCATIONS:
- Thoracic (60%)
- Lumbar (30%)
- Cervical (10%)
PRESENTATION:
- Pain: progressive, severe, radicular in pattern
- Weakness: typically progressive, symmetrical and pyramidal affecting extensors in UL and flexors in LL
- Disturbed gait
- Paraesthesia due to sensory disturbance (less common)
- If CES = unilateral symptoms of weakness, saddle anaesthesia, painless urinary retention and overflow incontinence + lower back pain (localised and radicular)
O/E:
- Increased tone if UMN lesion
- Hyper-reflexia below level of UMN lesion
- Positive Babinski sign
- If CES = LMN pattern, reduced anal tone on DRE, absent ankle jerk
INVESTIGATIONS:
- MRI of whole spine to identify the actual site of compression
- Other imaging options include bone scans, plain radiographs, CT scans and myelography
[NB: treat empirically before investigating]
Malignant Spinal Cord Compression: Principles of Management
GENERAL MEASURES:
- Emergency, for dexamethasone
- Analgesia for neuropathic pain (eg: amitryptyline)
- Bed rest, minimise movement to prevent pathological fractures
- VTE prophylaxis (eg: TED stockings, LMWH) if refractory pain due to increased VTE risk
- Catheterisation for painless urinary retention in CES
PHARMACOLOGICAL MEASURES:
- Dexamethasone 16mg stat as loading dose on initial assessment, followed by Dexamethasone 8mg BD to reduce oedema and relieve compression
RADIOTHERAPY:
- External beam radiotherapy for localised tumour control
- Stereotactic body radiotherapy (higher dose) to allow more targeted doses of radiotherapy directed at the tumour, while minimising exposure to surrounding tissue
SURGERY:
- Surgical decompression, reconstruction and vertebroplasty for unstable spines or radioresistant tumours
SVCO
- Definition
- Causes
- Presentation
- Examination
- Investigations and Diagnosis
DEFINITION AND AETIOLOGY:
- Obstruction of the SVC, which is a valveless structure
- Causes the formation of collateral vessels: azygous system, internal mammary and long thoracic system
[NB: collaterals take time to develop, therefore clinical features depend on time frame over which obstruction forms]
CAUSES:
a) Lung cancer
- NSCLC: < 2% of NSCLC will develop SVCO, but due to high incidence of NSCLC, it accounts for 50% of cases
- SCLC: note central position and rapid growth
b) Haematological cancer
- Non-hodgkin lymphoma (NHL)
c) Other cancers
- Thymic
- Breast
- Mediastinal germ tumours
- Direct tumour growth (rare)
- Lymphadenopathy (rare)
PRESENTATION:
- Dyspnoea
- Facial swelling
- “Fullness” of the head
- Symptoms worse on bending forth/lying down
- Cough
- Dysphagia
- Emergency: stridor, airway compromise, raised ICP causing coma and reduced cognition
O/E:
- Facial swelling
- Distended neck and chest wall veins
- UL oedema
- Facial plethora
- Cyanosis
- Cognitive dysfunction and coma
- Pemberton’s Sign (elevate both arms above head for 1-2 minutes, considered positive if it causes congestion, cyanosis or respiratory distress)
INVESTIGATIONS AND DIAGNOSIS:
a) Imaging
- CXR can demonstrate underlying lesion, mediastinal widening and malignant pleural effusion
- Contrast-enhanced CT chest can reveal level of obstruction and presence of collateral vessel formation
- PET-CT/CT abdo-pelvis or MRI brain can complete staging
- Duplex USS can identify SVCO, especially for those with indwelling catheters
b) Histopathology
- Minimally invasive procedures (eg: sputum/pleural fluid cytology, lymph node biopsy, bone marrow biopsies)
- Invasive procedures (eg: bronchoscopy, VATS)
[NB: biopsy should be guided by radiological findings]
SVCO:
- Emergency management
- Initial, general management
- Oncological management
- Surgical management
EMERGENCY MANAGEMENT:
- For respiratory distress or cerebral oedema
- Rarely needed
- Can present as airway obstruction (eg: stridor) or neurological symptoms consistent with cerebral oedema
- Consider diuretics and steroids
- Definitive management is with endovascular stent, shunt or thrombolysis if thrombus present
INITIAL GENERAL MANAGEMENT:
- Elevate the head and neck
- Oxygenate
- Dexamethasone 16mg stat as loading dose, followed by dexamethasone 8mg BD (TTD = 16mg) to reduce swelling
- Refer for stenting
ONCOLOGICAL TREATMENT:
- Radiotherapy usually effective as many tumours causing SVCO are radiosensitive, often first-line for NSCLC and lymphonas
- Chemotherapy can be considered for SCLC and NHL
- Anticoagulants or thrombolysis if SVCO due to intravascular thrombus
SURGICAL TREATMENT:
- Percutaneous insertion of endovascular stent (balloon expandable and self-expanding stents) via internal jugular, femoral or basilic veins has success rate of 95-100%
SVCO prognosis?
If SVCO is malignant, average life expectancy is 6 months
SVCO generally a negative prognostic indicator in terms of cancer survival
Bowel Obstruction:
- Physiology
- Common causes of BO
- Presentation and examination
- Investigation
PHYSIOLOGY:
- Occlusion leads to gross dilation of proximal limb of the bowel
- Peristalsis increases, leading to the secretion of a large volume of electrolyte-rich fluid into the bowel (ie: “third-spacing”) causing dehydration
COMMON CAUSES OF BO:
- Small bowel = adhesions post-op, hernia, malignancy
- Large bowel = malignancy, diverticular disease, volvulus
PRESENTATION:
- Abdominal pain: non-localised, colicky/cramping
- Vomiting: early if proximal obstruction, late if distal obstruction
- Absolute constipation: late if proximal obstruction, early if distal obstruction
- PMH reveals recent surgery or malignancy (eg: ovarian)
O/E:
- Signs of underlying cause: hernae, surgical scars
- Signs of deyhydration: prolonged CRT, pale cool extremeties, weak pulses, hypotension, dry and cracked oral mucosae
- Abdominal distention
- Focal tenderness, guarding
- Percussion of tympanic quality +/- percussion tenderness
- “Tinkling” high-pitched bowel sounds, sometimes reduced
INVESTIGATIONS:
a) Bloods
- Routine bloods
- Renal function and U&E for electrolyte derangement secondary to third-spacing
- G&S
- VBG for end-organ and metabolic derangement secondary to vomiting
- Lactate raised if ischaemic
b) Imaging
- CT abdomen with IV contrast is ideal
- AXR second-line (if SBO: >3cm, central with valvulae conniventes; if LBO: >6cm, peripheries with haustral lines)
Malignant Hypercalcaemia:
- Definition
- Classification
- Common Cancers
- Pathophysiology
- Presentation
- Investigations
DEFINITION:
- Serum corrected calcium concentration > 2.6 mmol/L
- Negative prognostic factor as it complicates 20-30% of malignancies
CLASSIFICATION:
- Mild: 2.6-3.0 mmol/L
- Moderate: 3.0-3.5 mmol/L
- Severe: > 3.5 mmol/L
COMMON CANCERS:
- Breast cancer
- Multiple myeloma
- Lymphoma
- Lung cancer (e.g. squamous cell carcinoma)
PATHOPHYSIOLOGY:
- PTHrP release from malignant cells stimulates PTH receptors, which work to increase bone resorption, distal tubular calcium absorption and inhibit proximal phosphate transport
- Osteolytic metastasis where deposition of tumour cells within bone leads to local production of cytokines and other mediators stimulating osteoclasts, leading to bone resorption
- Increased activated vitamin D levels lead to increased absorption of calcium from gastrointestinal enterocytes (eg: Hodgkin Lymphoma)
PRESENTATION:
“Stones (renal stones), bones (bone pain), thrones, abdominal groans and psychiatric moans (lethargy, fatigue, confusion, psychosis, depression)”
- Mild = Polyuria, Polydipsia, Mild cognitive impairment, Dyspepsia
- Moderate = Constipation, Weakness, Fatigue, Dehydration, Nausea
- Severe = Abdominal pain, Vomiting, Dysrhythmias (shortened QT interval, J waves, VF if severe), Pancreatitis, Coma
O/E:
- Reduced consciousness/cognition
- Signs of dehydration due to polyuria
INVESTIGATIONS:
a) Bedside
- ECGs to identify arrhythmias; common signs of hypercalcaemia include a shortened QT interval
b) Bloods
- Serum calcium to confirm hypercalcaemia
- Serum PTH = in malignancy, PTH should be low/suppressed; but if PTH is high, this suggests primary hyperparathyroidism and not malignancy
- Bone profile for derangement due to boney metastasis
- Myeloma screen (immunoglobulins, protein electrophoresis and urinary light chains)
- Serum vitamin D
c) Imaging
- CT/X-rays to identify malignant sources/lesions
- Parathyroid imaging to diagnose primary hyperparathyroidism (eg: neck ultrasound, Tc99m uptake scan)
Pleural Effusions:
- Pathophysiology
- Presentation and examination
- Investigations and interpretation
- Light’s Criteria
PATHOPHYSIOLOGY:
- Increased vasculature permeability (eg: malignancy) causing loss of fluid and macromolecules from ‘leaky’ vessels
- Increased microvascular pressure (eg: heart failure) increased venous pressure affects hydrostatic pressure forcing fluid out
- Decreased plasma oncotic pressure (eg: nephrotic syndrome, cirrhosis) which favours accumulation of fluid in the pleural space due to hypoproteinaemia
- Reduced lymphatic drainage due to infiltration (eg: cancer) or compression
PRESENTATION:
(onset < 24 hours)
- Breathlessness
- Non-productive cough
- Pleuritic chest pain
- Extra-pulmonary symptoms of malignancy (eg: weight loss)
[NB: onset is slower than in pulmonary embolism, which occurs suddenly, has associated haemoptysis and fever]
O/E:
- Reduced chest expansion
- Reduced breath sounds
- Stony dull percussion
- Reduced vocal resonance
- Trachea deviation (away from the side of effusion)
- Extra-pulmonary signs of malignancy (eg: finger clubbing in lung cancer)
INVESTIGATIONS:
- Chest X-ray all that is necessary
- USS can identify small effusions and guide aspiration
- Pleural paracentesis via USS guidance
INTERPETATION:
- Protein (transudate < 30g/L, exudate > 30g/L)
- pH
- Gram stain for bacteria
- MCS for infection
- LDH for malignancy and Light’s criteria
- Cytology for malignant cells
- Lipid testing: cholesterol, triglycerides
- Glucose
- Amylase
- Haematocrit
- Nucleated cell count
LIGHT’S CRITERIA:
Pleural fluid is an exudate if one or more of the following criteria are met:
- Pleural fluid protein:serum protein > 0.5
- Pleural fluid LDH:serum LDH >0.6
- Pleural fluid LDH >2/3 the upper limits of laboratory normal value for serum LDH
Venous Thromboembolism (VTE):
- Presentation and examination
- Investigations
- Management
PRESENTATION:
- Sudden onset dyspnoea
- Pleuritic chest pain, sharp, stabbing, unilateral
- Cough, or haemoptysis (rare)
O/E:
- Tachycardia
- Tachypnoea
- Pyrexia
- Raised JVP (rare)
- Pleural rub on auscultation
- Signs of DVT
INVESTIGATIONS:
- ECG to diagnose PE and to exclude MI; shows sinus tachycardia commonly, sometimes RBBB or RV strain (inverted T waves in V1-V4 and / or leads AvF-III), S1Q3T3 rare
- Well’s PE score ≤ 4: PE unlikely, perform D-dimers to exclude PE; however if D-dimer raised, then do CTPA
- Well’s PE score > 4: PE likely, for CTPA
- Well’s DVT score ≥ 2: DVT likely, for proximal leg vein USS scan
- Well’s DVT score ≤ 1: DVT unlikely, use D-dimers to exclude it
[NB: if USS is negative but D-dimer is still raised, repeat USS in 6-8 days]
MANAGEMENT:
- Either DOACs or LMWH (eg: dalteparin) as recommended by NICE; treatment to last for 6 months in unprovoked DVT as in the case of cancer (provoked DVTs would be 3 months)
- For DOACs, check renal function, consider risk of bleeding (higher risk) and also look at issues with the clotting cascade (eg: low platelets)
- ???LMWH alone is recommended for cancer-associated VTE, due to lower recurrence rates than on Warfarin
- If considering Warfarin, for therapeutic LMWH cover until the INR levels are sufficiently therapeutic
- Anticoagulation treatment should be continued for 3 months in those with a provoked DVT, lifelong anticoagulation may be needed indefinitely
Gastrointestinal Bleeding:
- Causes
- Presentation
- Investigations
- Scoring systems and application
CAUSES:
- Peptic ulcers (the most common cause)
- Mallory-Weiss tear
- Oesophageal varices (secondary to portal hypertension in liver cirrhosis/cancer)
- Stomach cancers
PRESENTATION;
- Haematemesis of “coffee-brown” colour
- Melaena (tarry, black and greasy, offensive-smelling stools)
- Oesophageal varices may reveal ascites, jaundice and caput medusae
- Stomach cancer patients may present with weight loss, epigastric pain, treatment-resistant dyspepsia, low haemoglobin (anaemia) and a raised platelet count
- PMH may reveal NSAID/aspirin use, or DOACs/Warfarin
- SHX may reveal smoking/alcoholism (increased risk of peptic ulceration)
O/E:
- Haemodynamic instability (tachycardia, hypotension, cold and clammy extremities)
- Low urine output
- Low JVP
- “JACCCL” signs of underlying malignancy (eg: jaundice, anaemia, clubbing and cirrhosis, cyanosis and lymphadenopathy)
- DRE may reveal PR bleeding
INVESTIGATIONS:
a) Bloods
- Urate may be high due to protein (blood) digestion
- FBC may reveal low Hb
- LFTs deranged if hepatic malignancy
- U&Es deranged if dehydrated
- G&S necessary for surgery and transfusion
- Crossmatch
- Clotting studies (PT, APTT, INR)
b) Imaging
- Endoscopy (urgent < 24 hours)
c) Scoring systems
- Glasgow-Blatchford score to estimate chance of UGIB
- Rockall score to estimate risk of bleeding following endoscopy
GLASGLOW-BLATCHFORD SCORE:
(Ues to predict the likelihood of a patient having a UGIB based on clinical presentation; score of > 0 indicates high risk)
“BLEEDS” mnemonic
- BP low
- Low Hb
- Elevated heart rate
- Elevated urea
- Dark tarry stools of melaena
- Syncope
ROCKALL SCORE:
(Calculates percentage risk of re-bleeding and mortality for those with confirmed UGIB, and who have undergone endoscopy)
“ROCKALL” mnemonic
- Racing heart of tachycardia
- Oncological cause of bleed (malignancy)
- Co-morbidities
- Kincking (mallory-weiss tear)
- Age
- Low BP
- Looks like they bled on endoscopy
Bowel Obstruction: Principles of Management
INITIAL MEASURES:
- NBM
- IV fluids for dehydration
- NGT
- Catheterise and monitor input-output balance
CONSERVATIVE:
- “Drip and suck” = IV fluids (drip) to correct electrolyte disturbances, NGT (suck) to decompress the bowel
- Anti-emetics: cyclizine (H1 antagonist at CTZ) to alleviate vomiting
- Dexamethasone to reduce oedema and inflammation
- Analgesia: oxycodone for pain control
- Buscopan for smooth muscle spasms
- Octreotide to reduce secretions
SURGERY:
- Indicated if ischaemic (raised lactate), closed loop obstruction, hernia, failure to resolve with conservative measures
- Laparotomy by default
- Defunctioning stoma necessary
Malignant Hypercalcaemia: Principles of management
ASYMPTOMATIC AND CORRECTED CA2+ < 3.0mmol/L:
- Encourage oral hydration
- If dehydrated, for IV 0.9% Sodium Chloride, then recheck corrected Ca2+ after 24 hours of hydration
- If Ca2+ still elevated, then treat as symptomatic hypercalcaemia
SYMPTOMATIC AND/OR CORRECTED CA2+ > 3.0mmol/L:
a) Stop
- Thiazide diuretics
- Vitamin D and calcium supplements
- Nephrotoxic drugs (eg: diuretics, ACEi, NSAIDS)
b) Start
- IV 0.9% Sodium Chloride at a rate of 3 litres over 24 hours, aiming for urine output of 100‐150ml/hour
- Zoledronic acid commenced after 12-24h after hydration =, at a rate adjusted for renal function (see below*)
- Recheck corrected calcium in 4 days to monitor the effect of the Zoledronic Acid. Continue rehydration and recheck U&Es
- Seek specialist advice if hypercalcaemia continues after day 4
[NB: zoledronic acid is a bisphosphonate which binds Ca2+]
IV ZOLENDRONIC ACID RATES OF INFUSION:
- eGFR> 60ml/min: 4mg in 100ml 0.9% Sodium Chloride over 15 minutes
- eGFR 50‐60ml/min: 3.5mg in 100ml 0.9% Sodium Chloride over 15 minutes
- eGFR 40‐50ml/min: 3.3mg in 100ml 0.9% Sodium Chloride over 15 minutes
- eGFR 30‐40ml/min: 3mg in 100ml 0.9% Sodium Chloride over 15 minutes
- eGFR < 30ml/min: not routinely recommended, seek specialist advice
NB: if renal failure, not for zolendronic acid, give pamidronate instead
Pleural Effusions: Principles of Management
ADDRESS UNDERLYING CAUSE:
- Treat underlying malignancy, discuss in MDT
PLEURAL ASPIRATION +/- CHEST DRAINS:
- Therapeutic paracentesis which involves the removal of 1-1.5 L of pleural fluid via a special drainage kit
- Chest drain insertion which involves the insertion of a tube (10-14 Fr) into the pleural space to allow drainage over hours to days. Drains are connected to an underwater seal to prevent the backflow of air or fluid into the pleural space
PLEURODESIS:
- A procedure to obliterate the pleural space and prevent re-accumulation of fluid or air
- Uses chemical sclerosants
- Video-assisted thoracoscopic surgery
Pleural Effusions: Complications with chest drain insertion or paracentesis?
- Re-expansion pulmonary oedema: this refers to the development of pulmonary oedema on re-expansion of the lung. To reduce the risk patients should be monitored for symptoms and drainage limited to 1-1.5 L at any time. If symptoms develop at a lower drainage volume, the drain can be clamped and patients reassessed before continuation.
- Pneumothorax: patients may have a post-procedure pneumothorax due to iatrogenic lung puncture or inadvertent introduction of air
- Infection: a complicated parapneumonic pleural effusion may develop from poor sterile technique
Bleeding - Damage to thoracic viscera
Subcutaneous emphysema
Gastrointestinal Bleeding: Principles of management
“ABATED”
A – ABCDE approach to immediate resuscitation
B – Bloods to include Hb, urea, G&S, crossmatch, coagulation and LFTs
A – Access (ideally 2 x large bore cannula)
T – Transfusions of bloods, clotting factors and platelets
E – Endoscopy (within 24 hours)
D – Drugs (stop anticoagulants and NSAIDs)
STOP:
- Antigoagulants
- NSAIDs and aspirin
START:
- PPi (NICE discourages it)
- Terlipressin if chronic liver disease
- Antibiotics due to risk of infectious bacteraemia
- Beta-blockers to decrease BP of blood flowing through azygos veins, thereby decreasing risk of variceal bleed
- FFP (KIV if INR > 1.8)
- Vitamin K (KIV if INR > 1.8)
Adrenal Crisis due to Adrenal Metastasis:
- Subtypes
- Presentation
- Investigations
- Management
SUBTYPES:
- Primary adrenal insufficiency = due to adrenal gland damage and subsequent lack of cortisol and aldosterone
- Secondary adrenal insufficiency = due to insufficient ACTH and therefore lack of adrenal stimulation; most commonly due to pituitary damage (eg: pituitary adenoma, Sheeshan’s syndrome)
PRESENTATION:
(vague symptoms)
- Fatigue
- Muscle weakness
- Muscle cramps
- Dizziness and fainting
- Thirst and craving salt (due to lack of aldosterone and salt wasting)
- Weight loss
- Abdominal pain
- Depression
- Reduced libido
[NB: history may reveal a steroid-dependant patient who forgets to take their medications; or a patient with adrenal metastases]
O/E:
- Bronze hyperpigmentation of the hands/skin, particularly in creases (ACTH stimulates melanocytes to produce melanin)
- Hypotension (esp postural hypotension)
INVESTIGATIONS:
a) Bloods
- U&Es likely to reveal hyponatraemia; other findings include hyperkalaemia
- Serum calcium may show hypercalcaemia
- BM may reveal hypoglycaemia
b) Short synacthen test
- Synacthen is a synthetic analogue of ACTH
- Perform in the morning
- Give a dose of synacthen (synthetic ACTH), which should stimulate the adrenal gland to synthesise cortisol, then measure serum cortisol 30 mins and 60 mins later; it should roughly double in normal cases
- If cortisol fails to double, it indicates either primary adrenal insufficiency (due to malignancy) or significant adrenal atrophy after a prolonged absence of ACTH in secondary adrenal insufficiency
c) Imaging
- CT or MRI of the adrenal glands to identify adrenal tumours
- MRI of the pituitary gland to identify pituitary adenoma
MANAGEMENT:
- Hydrocortisone 100mg stat, followed by hydrocortisone 50mg QDS (as per Adrenal crisis management)
