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Malignant hyperpyrexia
complication of general anesthesia
characterised by hyperpyrexia and muscle rigidity
susceptibility to malignant hyperthermia is inherited in an autosomal dominant fashion
Cause agents of Malignant hyperpyrexia
halothane
suxamethonium
other drugs: antipsychotics (neuroleptic malignant syndrome)
Investigations and management Malignant hyperpyrexia
nvestigations
CK raised
contracture tests with halothane and caffeine
Management
dantrolene - prevents Ca2+ release from the sarcoplasmic reticulum
Pericarditis
Features
chest pain: may be pleuritic. Is often relieved by sitting forwards
other symptoms include non-productive cough, dyspnoea and flu-like symptoms
pericardial rub
tachypnoea
tachycardia
Pericarditis causes
Causes viral infections (Coxsackie) tuberculosis uraemia (causes 'fibrinous' pericarditis) trauma post-myocardial infarction, Dressler's syndrome connective tissue disease hypothyroidism malignancy
Pericarditis ECG
nvestigations
ECG changes
the changes in pericarditis are often global/widespread, as opposed to the ‘territories’ seen in ischaemic events
‘saddle-shaped’ ST elevation
PR depression: most specific ECG marker for pericarditis
all patients with suspected acute pericarditis should have transthoracic echocardiography
Pericarditis management
treat the underlying cause
a combination of NSAIDs and colchicine is now generally used for first-line for patients with acute idiopathic or viral pericarditis
complications of MI
Acute mitral regurgitation - cute hypotension and pulmonary oedema may occur. An early-to-mid systolic murmur is typically heard.
Ventricular septal defect - Rupture of the interventricular septum usually occurs in the first week and is seen in around 1-2% of patients. Features: acute heart failure associated with a pan-systolic murmur. An echocardiogram is diagnostic and will exclude acute mitral regurgitation which presents in a similar fashion. Urgent surgical correction is needed.
Left ventricular free wall rupture - 3% of MIs and occurs around 1-2 weeks afterwards. Patients present with acute heart failure secondary to cardiac tamponade (raised JVP, pulsus paradoxus, diminished heart sounds)
Dressler’s syndrome tends to occur around 2-6 weeks following a MI. The underlying pathophysiology is thought to be an autoimmune reaction against antigenic proteins formed as the myocardium recovers. It is characterised by a combination of fever, pleuritic pain, pericardial effusion and a raised ESR. It is treated with NSAIDs.
Upper gastrointestinal bleeding presentation
Patients may present with the following:
Haematemesis and/ or malaena
Epigastric discomfort
Sudden collapse
Duodenum ulcer- Upper GI bleed
major haemorrhage is a posteriorly sited duodenal ulcer - erode the gastroduodenal artery
Pain occurs several hours after eating.
Management of upper GI bleed
Admission to hospital careful monitoring, cross match blood, check FBC, LFTs, U+E and Clotting (as a minimum)
Patients with on-going bleeding and haemodynamic instability are likely to require O negative blood pending cross matched blood
Early control of airway is vital (e.g. Drowsy patient with liver failure)
Patients with suspected varices should receive terlipressin prior to endoscopy
upper gastrointestinal haemorrhage should undergo Upper GI endoscopy within 24 hours of admission. In those who are unstable this should occur immediately after resuscitation or in tandem with it. The endoscopy department is a potentially dangerous place for unstable patients and it may be safer to perform the endoscopy in theatre with an anaesthetist present.
Varices should be banded or subjected to sclerotherapy. If this is not possible owing to active bleeding then a Sengaksten- Blakemore tube (or Minnesota tube) should be inserted. This should be done with care; gastric balloon should be inflated first and oesophageal balloon second. Remember the balloon with need deflating after 12 hours (ideally sooner) to prevent necrosis. Portal pressure should be lowered by combination of medical therapy +/- TIPSS.
Surgery
Duodenal ulcer
Laparotomy, duodenotomy and under running of the ulcer. If bleeding is brisk then the ulcer is almost always posteriorly sited and will have invaded the gastroduodenal artery. Large bites using 0 Vicryl are taken above and below the ulcer base to occlude the vessel. The duodenotomy should be longitudinal but closed transversely to avoid stenosis.
For gastric ulcer
Under-running of the bleeding site
Partial gastrectomy-antral ulcer
Partial gastrectomy or under running the ulcer- lesser curve ulcer (involving left gastric artery)
Total gastrectomy if bleeding persists
Oesophagitis presentation
Small volume of fresh blood, often streaking vomit. Malaena rare. Often ceases spontaneously. Usually history of antecedent GORD type symptoms.
Upper GI Cancer presentation
Usually small volume of blood, except as pre terminal event with erosion of major vessels. Often associated symptoms of dysphagia and constitutional symptoms such as weight loss. May be recurrent until malignancy managed.
Mallory Weiss Tear presentation
Typically brisk small to moderate volume of bright red blood following bout of repeated vomiting. Malaena rare. Usually ceases spontaneously.
Varices presentation
Usually large volume of fresh blood. Swallowed blood may cause malaena. Often associated with haemodynamic compromise. May stop spontaneously but re-bleeds are common until appropriately managed.
Gastric cancer presentation
May be frank haematemesis or altered blood mixed with vomit. Usually prodromal features of dyspepsia and may have constitutional symptoms. Amount of bleeding variable but erosion of major vessel may produce considerable haemorrhage.
Dieulafoy Lesion presentation
Often no prodromal features prior to haematemesis and malaena, but this arteriovenous malformation may produce quite considerable haemorrhage and may be difficult to detect endoscopically
Gastric ulcer presentation
Small low volume bleeds more common so would tend to present as iron deficiency anaemia. Erosion into a significant vessel may produce considerable haemorrhage and haematemesis.
Hyperosmolar hyperglycaemia clinical features
high blood sugar results in high osmolarity without significant ketoacidosis
HHS = medical emergency
Clinical features
General: fatigue, lethargy, nausea and vomiting
Neurological: altered level of consciousness, headaches, papilloedema, weakness
Haematological: hyperviscosity (may result in myocardial infarctions, stroke and peripheral arterial thrombosis)
Cardiovascular: dehydration, hypotension, tachycardia
Hyperosmolar hyperglycaemia diagnosis
Diagnosis
1. Hypovolaemia
2. Marked Hyperglycaemia (>30 mmol/L) without significant ketonaemia or acidosis
3. Significantly raised serum osmolarity (> 320 mosmol/kg)
Note: A precise definition of HHS does not exist, however the above 3 criteria are helpful in distinguishing between HHS and DKA. It is also important to remember that a mixed HHS / DKA picture can occur.
HHS management
The goals of management of HHS can be summarised as follows:
- Normalise the osmolality (gradually)
- Replace fluid and electrolyte losses
- Normalise blood glucose (gradually)
Fluid replacement
Fluid losses in HHS are estimated to be between 100 - 220 ml/kg (e.g. 10-22 litres in an individual weighing 100 kg).
Intravenous (IV) 0.9% sodium chloride solution is the first line fluid for restoring total body fluid.
If the serum osmolarity is not declining despite positive balance with 0.9% sodium chloride, then the fluid should be switched to 0.45% sodium chloride solution which is more hypotonic relative to the HHS patients serum osmolarity
Fluid replacement alone (without insulin) will gradually lower blood glucose which will reduce osmolality
Rapid changes must be avoided. A safe rate of fall of plasma glucose of between 4 and 6 mmol/hr is recommended. The rate of fall of plasma sodium should not exceed 10 mmol/L in 24 hours.
A target blood glucose of between 10 and 15 mmol/L is a reasonable goal.
Complete normalisation of electrolytes and osmolality may take up to 72 hours.
If significant ketonaemia is present (3β-hydroxy butyrate is more than 1 mmol/L) this indicates relative hypoinsulinaemia and insulin should be started at time zero (e.g. mixed DKA / HHS picture). The recommended insulin dose is a fixed rate intravenous insulin infusion given at 0.05 units per kg per hour.
If significant ketonaemia is not present (3β-hydroxy butyrate is less than 1 mmol/L) then do NOT start insulin.
- ovarian teratoma
teratomas comprise dermal, mesodermal and endodermal elements
well-differentiated derivations from at least two of the three germ cell layers (i.e. ectoderm, mesoderm, and endoderm).
USS
chogenic mass with posterior sound attenuation
chogenic, shadowing calcific or dental (tooth) components
luid-fluid levels
multiple thin, echogenic bands caused by the hair in the cyst cavity: the dot-dash pattern (dermoid mesh)
ie Unilocular cyst with a solid intracavitary mass containing hair, skin with subcutis, bone and cartilage
dermoid
dermoid is composed only of dermal and epidermal elements (which are both ectodermal in origin),
Follicular cyst
Rarely greater than 8 cm Glistening membrane Thin walled Unilocular or multilocular Clear or serous fluid contents No solid component
Serous cystadenoma
most common ovarian neoplasm,
unilocular (or at times multilocular) cysts filled with clear watery fluid. The cysts measure 10 cm in average diameter but may be extremely large.
Mucinous cystadenoma
benign cystic tumor lined by a mucinous epithelium.
multilocular cyst with smooth outer and inner surfaces. It tends to be huge in size.
simple cyst management
A pelvic ultrasound is the single most effective way of evaluating an ovarian mass with transvaginal ultrasonography being preferable due to its increased sensitivity over transabdominal ultrasound.
Women with small (less than 50 mm diameter) simple ovarian cysts generally do not require follow-up as these cysts are very likely to be physiological and almost always resolve within 3 menstrual cycles.
Women with simple ovarian cysts of 50–70 mm in diameter should have yearly ultrasound follow-up and those with larger simple cysts should be considered for either further imaging (MRI) or surgical intervention.
Alcohol units calculation
multiplying the total volume of a drink (in ml) by its ABV (measured as a percentage) and dividing the result by 1,000
Pulmonary hypertension
What is this
Pulmonary hypertension is an increase of blood pressure in the pulmonary artery, pulmonary vein, or pulmonary capillaries, together known as the lung vasculature, leading to shortness of breath, dizziness, fainting, leg swelling and other symptoms.
Pulmonary hypertension pressure and causes
= mean pulmonary arterial pressure that is greater than 25 mmHg.
causes by heart failure, chronic lung disease
chronic thromboembolic pulmonary hypertension
Pulmonary hypertension presentation
Presentation Symptoms exertional dyspnea, chest pain, and syncope fatigue and lethargy Physical examination loud P2 on auscultation right ventricular heave right-sided 4th heart sound murmurs holosystolic murmur of tricuspid regurgitation systolic ejection murmur diastolic pulmonic regurgitation (in severe cases)
Pulmonary hypertension treatment
Treatment
Conservative
continuous long-term oxygen therapy
indication
to maintain adequate oxygenation
Medical
note that there are a myriad of causes of pulmonary hypertension
treatment should be aimed at treating and optimizing the underlying condition (e.g., anticoagulation in patients with recurrent pulmonary embolisms)
vasoactive agents
indication
pulmonary hypertension targeted therapy
medication options
calcium channel blockers
prostacyclin pathway agonists (e.g., epoprostenol, treprostinil, and iloprost)
endothelin receptor antagonists (e.g., bosentan, macitentan, and ambrisentan)
nitric oxide-cyclic GMP enhancer (e.g., sildenafil and tadalafil)
Myeloma presentation
The median age at presentation is 70-years-old.
Use the mnemonicCRABBI:
Calcium - Hypercalcaemia occurs as a result of increased osteoclast activity within the bones
This leads to constipation, nausea, anorexia and confusion
Renal
Monoclonal production of immunoglobulins results in light chain deposition within the renal tubules
This causes renal damage which presents as dehydration and increasing thirst
Other causes of renal impairment in myeloma include amyloidosis, nephrocalcinosis, nephrolithiasis
Anaemia
Bone marrow crowding suppresses erythropoiesis leading to anaemia
This causes fatigue and pallor
Bleeding
bone marrow crowding also results in thrombocytopenia which puts patients at increased risk of bleeding and bruising
Bones
Bone marrow infiltration by plasma cells and cytokine-mediated osteoclast overactivity creates lytic bone lesions
This may present as pain (especially in the back) and increases the risk of fragility fractures
Infection
a reduction in the production of normal immunoglobulins results in increased susceptibility to infection
Myeloma investigations
Investigations
Bloods will show anaemia (FBC) and thrombocytopenia (FBC); raised urea and creatinine (U&E) and raised calcium
Peripheral blood film: rouleaux formation
Serum or urine protein electrophoresis: raised concentrations of monoclonal IgA/IgG proteins will be present in the serum. In the urine, they are known as Bence Jones proteins
Bone marrow aspiration and trephine biopsy: confirms the diagnosis if the number of plasma cells is significantly raised
Whole-body MRI (or CT if MRI is not suitable) is used to survey the skeleton for bone lesions
Myeloma diagnosis
Symptomatic multiple myeloma is defined at diagnosis by the presence of the following three factors:
Monoclonal plasma cells in the bone marrow >10%
Monoclonal protein within the serum or the urine (as determined by electrophoresis)
Evidence of end-organ damage e.g. hypercalcaemia, elevated creatinine, anaemia or lytic bone lesions/fractures
myeloma management
For patients who are suitable for autologous stem cell transplantation* induction therapy consists of Bortezomib + Dexamethasone
For patients who are unsuitable for autologous stem cell transplantation*, induction therapy consists of Thalidomide + an Alkylating agent + Dexamethasone
Pain: treat with analgesia (using the WHO analgesic ladder)
Pathological fracture: Zoledronic acid is given to prevent and manage osteoporosis and fragility fractures as these are a large cause of morbidity and mortality, particularly in the elderly.
Infection: patients receive annual influenza vaccinations. They may also receive Immunoglobulin replacement therapy.
VTE prophylaxis
Fatigue: treat all possible underlying causes. If symptoms persist consider an erythropoietin analogue.
