Conditions Flashcards
Wrist Drop
Radial nerve palsy
Claw Hand
Ulnar Nerve Damage
Hand of Benediction
Median Nerve palsy
Radiculopathy
Pinched Nerve
Radiculopathy is most commonly a result of nerve compression, which can be caused by:
Intervertebral disc prolapse
The lumbar spine is predominantly affected by repeated minor stresses that predispose to rupture of the annulus fibrosus and sequestration of disc material (the nucleus pulposus)
Degenerative diseases of the spine – leading to neuroforaminal or spinal canal stenosis
The cervical spine is the most mobile segment of the spine and degenerative change is a normal part of ageing process; 80% of the population over 55 years old have degenerative changes between C5/6 and C6/7
Fracture – either trauma or pathological
Malignancy – most commonly metastatic
Infection – such as extradural abscesses, osteomyelitis (most commonly tuberculosis (‘Pott’s disease’)), or Herpes Zoster
Clinical features of radiculopathy include sensory features (paraesthesia and numbness) and motor features (weakness). Radicular pain is often also present, typically described as a burning, deep, strap-like, or narrow pain. It is not uncommon for radicular pain to be intermittent.
The ‘red flag’ symptoms* (Table 1) should also be specifically asked in patients with this presenting symptom, as they may indicate emergency or sinister pathology.
On examination, it is important to identify dermatomal and myotomal involvement. Ensure to evaluate for cauda equina syndrome, by assessing for pinprick sensation in the perianal dermatomes (reduced in CES), anocutaneous reflex (diminished or absent in CES), anal tone (reduced in CES), and rectal pressure sensation (reduced in CES).
Symptomatic Management
Analgesia is an important aspect of management in these patients. The WHO analgesic ladder can be utilised in the first instance, however neuropathic pain medications are frequently utilised.
Amitriptyline is usually first line, or pregabalin and gabapentin as alternatives. The patients may also suffer from muscle spasms and these can be managed with benzodiazepines (often diazepam) or baclofen.
Physiotherapy remains an important part of management in this patient group.
End of Life Medicine
Morphine sulfate 5mg sub cut as required for pain, cough and breathlessness
Midazolam 5mg sub cut as required for agitation and breathlessness
Hyoscine butylbromide 20mg sub cut as required for respiratory secretions
Levomepromazine 5mg sub cut as required for nausea
Levomepromazine 25mg sub cut as required for severe agitation
Hypocalcemia
As extracellular calcium concentrations are important for muscle and nerve function many of the features seen in hypocalcaemia seen a result of neuromuscular excitability
Features
tetany: muscle twitching, cramping and spasm
perioral paraesthesia
if chronic: depression, cataracts
ECG: prolonged QT interval
Trousseau’s sign
carpal spasm if the brachial artery occluded by inflating the blood pressure cuff and maintaining pressure above systolic
wrist flexion and fingers are drawn together
seen in around 95% of patients with hypocalcaemia and around 1% of normocalcaemic people
Chvostek’s sign
tapping over parotid causes facial muscles to twitch
seen in around 70% of patients with hypocalcaemia and around 10% of normocalcaemic people
The clinical history combined with parathyroid hormone levels will reveal the cause of hypocalcaemia in the majority of cases
Causes
vitamin D deficiency (osteomalacia)
chronic kidney disease
hypoparathyroidism (e.g. post thyroid/parathyroid surgery)
pseudohypoparathyroidism (target cells insensitive to PTH)
rhabdomyolysis (initial stages)
magnesium deficiency (due to end organ PTH resistance)
massive blood transfusion
acute pancreatitis
Contamination of blood samples with EDTA may also give falsely low calcium levels.
Management
severe hypocalcaemia (e.g. carpopedal spasm, tetany, seizures or prolonged QT interval) requires IV calcium replacement
the preferred method is with intravenous calcium gluconate, 10ml of 10% solution over 10 minutes
intravenous calcium chloride is more likely to cause local irritation
ECG monitoring is recommended
further management depends on the underlying cause
Hypercalcemia
The initial management of hypercalcaemia is rehydration with normal saline, typically 3-4 litres/day. Following rehydration bisphosphonates may be used. They typically take 2-3 days to work with maximal effect being seen at 7 days
Other options include:
calcitonin - quicker effect than bisphosphonates
steroids in sarcoidosis
Loop diuretics such as furosemide are sometimes used in hypercalcaemia, particularly in patients who cannot tolerate aggressive fluid rehydration. However, they should be used with caution as they may worsen electrolyte derangement and volume depletion.
Hypokalaemia
Potassium and hydrogen can be thought of as competitors. Hyperkalaemia tends to be associated with acidosis because as potassium levels rise fewer hydrogen ions can enter the cells
Hypokalaemia with alkalosis
vomiting
thiazide and loop diuretics
Cushing’s syndrome
Conn’s syndrome (primary hyperaldosteronism)
Hypokalaemia with acidosis
diarrhoea
renal tubular acidosis
acetazolamide
partially treated diabetic ketoacidosis
Magnesium deficiency may also cause hypokalaemia. In such cases, normalizing the potassium level may be difficult until the magnesium deficiency has been corrected
For exams it is useful to be able to classify the causes of hypokalaemia in to those associated with hypertension, and those which are not
Hypokalaemia with hypertension
Cushing’s syndrome
Conn’s syndrome (primary hyperaldosteronism)
Liddle’s syndrome
11-beta hydroxylase deficiency*
Carbenoxolone, an anti-ulcer drug, and liquorice excess can potentially cause hypokalaemia associated with hypertension
Hypokalaemia without hypertension
diuretics
GI loss (e.g. Diarrhoea, vomiting)
renal tubular acidosis (type 1 and 2**)
Bartter’s syndrome
Gitelman syndrome
*21-hydroxylase deficiency, which accounts for 90% of congenital adrenal hyperplasia cases, is not associated with hypertension
**type 4 renal tubular acidosis is associated with hyperkalaemia
Hyperkalaemia
Plasma potassium levels are regulated by a number of factors including aldosterone, acid-base balance and insulin levels. Metabolic acidosis is associated with hyperkalaemia as hydrogen and potassium ions compete with each other for exchange with sodium ions across cell membranes and in the distal tubule. ECG changes seen in hyperkalaemia include tall-tented T waves, small P waves, widened QRS leading to a sinusoidal pattern and asystole
Causes of hyperkalaemia:
acute kidney injury
drugs*: potassium sparing diuretics, ACE inhibitors, angiotensin 2 receptor blockers, spironolactone, ciclosporin, heparin**
metabolic acidosis
Addison’s disease
rhabdomyolysis
massive blood transfusion
Foods that are high in potassium:
salt substitutes (i.e. Contain potassium rather than sodium)
bananas, oranges, kiwi fruit, avocado, spinach, tomatoes
*beta-blockers interfere with potassium transport into cells and can potentially cause hyperkalaemia in renal failure patients - remember beta-agonists, e.g. Salbutamol, are sometimes used as emergency treatment
**both unfractionated and low-molecular weight heparin can cause hyperkalaemia. This is thought to be caused by inhibition of aldosterone secretion
Hyponatraemia
Hyponatraemia may be caused by water excess or sodium depletion. Causes of pseudohyponatraemia include hyperlipidaemia (increase in serum volume) or a taking blood from a drip arm. Urinary sodium and osmolarity levels aid making a diagnosis
Urinary sodium > 20 mmol/l
Sodium depletion, renal loss (patient often hypovolaemic)
diuretics: thiazides, loop diuretics
Addison’s disease
diuretic stage of renal failure
Patient often euvolaemic
SIADH (urine osmolality > 500 mmol/kg)
hypothyroidism
Urinary sodium < 20 mmol/l
Sodium depletion, extra-renal loss
diarrhoea, vomiting, sweating
burns, adenoma of rectum
Water excess (patient often hypervolaemic and oedematous)
secondary hyperaldosteronism: heart failure, liver cirrhosis
nephrotic syndrome
IV dextrose
psychogenic polydipsia
Hyponatraemia: treatment
Untreated, severe hyponatraemia may result in cerebral oedema, which in turn can cause brain herniation. It is therefore important to promptly identify and treat hyponatremia appropriately. However, the particular management for each patient is based on a number of factors listed below. Further to this, over-rapid correction may result in osmotic demyelination syndrome.
Principles
Management of hyponatremia is complicated and primarily based on the following parameters:
duration of hyponatremia: is it acute or chronic?
acute: develops over a period of < 48 hours
chronic: develops over a period > 48 hours
the severity of hyponatremia: what is the sodium level?
mild: 130-134 mmol/L
moderate: 120-129 mmol/L
severe: < 120 mmol/L
symptoms: is the patient symptomatic?
patients with mild hyponatraemia may be symptomatic
early symptoms may include: headache, lethargy, nausea, vomiting, dizziness, confusion, and muscle cramps
late symptoms may include: seizures, coma, and respiratory arrest
the suspected aetiology of the hyponatraemia:
hypovolemic hyponatraemia/clinically dehydrated: diuretic stage of renal failure, diuretics, Addisonian crisis
euvolemic hyponatraemia: SIADH
hypervolaemic hyponatraemia: heart failure, liver failure, nephrotic syndrome
Management
Initial steps in all patients
exclude a spurious result (e.g. blood taken from a drip arm)
review medications that may cause hyponatraemia
Chronic hyponatreamia without severe symptoms
If a hypovolemic cause is suspected
normal, i.e. isotonic, saline (0.9% NaCl)
this may sometimes be given as a trial
if the serum sodium rises this supports a diagnosis of hypovolemic hyponatraemia
if the serum sodium falls an alternative diagnosis such as SIADH is likely
If a euvolemic cause is suspected
fluid restrict to 500–1000 mL/day
consider medications:
demeclocycline
vaptans (see below)
If a hypervolemic cause is suspected
fluid restrict to 500–1000 mL/day
consider loop diuretics
consider vaptans
Acute hyponatreamia with severe symptoms
Patients with acute, severe (<120 mmol/L) or symptomatic hyponatraemia require close monitoring, preferably in an HDU or above setting.
Hypertonic saline (typically 3% NaCl) is used to correct the sodium level more quickly than would be done in patients with chronic hyponatraemia.
Notes on specific medications
Vasopressin/ADH receptor antagonists (vaptans):
these act primarily on V2 receptors - antagonism of V2 receptors results in selective water diuresis, sparing the electrolytes
They should be avoided in patients who have hypovolemic hyponatremia
Vasopression/ADH receptor antagonists can stimulate the thirst receptors leading to the desire to drink free water. They can be hepatotoxic in patients with underlying liver disease.
Complications of treatment
Osmotic demyelination syndrome (central pontine myelinolysis)
can occur due to over-correction of severe hyponatremia
to avoid this, Na+ levels are only raised by 4 to 6 mmol/l in a 24-hour period
symptoms usually occur after 2 days and are usually irreversible: dysarthria, dysphagia, paraparesis or quadriparesis, seizures, confusion, and coma
patients are awake but are unable to move or verbally communicate, also called ‘Locked-in syndrome’
Hypophosphataemia
Causes
alcohol excess
acute liver failure
diabetic ketoacidosis
refeeding syndrome
primary hyperparathyroidism
osteomalacia
Consequences
red blood cell haemolysis
white blood cell and platelet dysfunction
muscle weakness and rhabdomyolysis
central nervous system dysfunction
SIADH
Syndrome of inappropriate ADH secretion
The syndrome of inappropriate ADH secretion (SIADH) is characterised by hyponatraemia secondary to the dilutional effects of excessive water retention. Patients with SIADH are typically euvolemic, i.e. they do not show signs of overt volume depletion or overload.
Pathophysiology
SIADH involves an excessive release of antidiuretic hormone (ADH), also known as vasopressin, which leads to water retention, volume expansion, and dilutional hyponatraemia
ADH is produced by the hypothalamus and stored in the posterior pituitary gland. Its primary function is to regulate the body’s water balance
It does this by increasing water reabsorption in the collecting ducts of the kidneys, thereby decreasing the volume of urine produced
In SIADH, there is an inappropriate and continuous release of ADH that is not inhibited by normal physiological mechanisms, such as adequate or excess body fluid levels
As a result, the kidneys reabsorb more water, leading to decreased urine output, and expansion of extracellular fluid volume.
Importantly, this increase in body fluid volume does not lead to the expected signs of fluid overload, such as oedema or hypertension, because the excess fluid is uniformly distributed throughout all body fluid compartments.
However, as water is retained in the body, the concentration of electrolytes in the blood, particularly sodium, becomes diluted, leading to hyponatraemia.
Causes of SIADH
Category Examples
Malignancy
small cell lung cancer
also: pancreas, prostate
Neurological
stroke
subarachnoid haemorrhage
subdural haemorrhage
meningitis/encephalitis/abscess
Infections
tuberculosis
pneumonia
Drugs
sulfonylureas*
SSRIs, tricyclics
carbamazepine
vincristine
cyclophosphamide
Other causes
positive end-expiratory pressure (PEEP)
porphyrias
Investigations
Urine osmolality: Urine osmolality is inappropriately high (>100 mOsm/kg) in relation to serum osmolality, as the kidneys should normally dilute urine in the setting of low serum osmolality.
Urine sodium concentration: Urine sodium concentration is typically high (>40 mmol/L) due to the action of ADH on the renal tubules.
Management
correction must be done slowly to avoid precipitating central pontine myelinolysis
fluid restriction
demeclocycline: reduces the responsiveness of the collecting tubule cells to ADH
ADH (vasopressin) receptor antagonists have been developed
*the BNF states this has been reported with glimepiride and glipizide.
