Electrolyes Flashcards
Treatment of SIADH
Demeclocycline TolvAptan Conivaptan Lithium Urea
Vaptans are V2 receptor antagonists
- specific and work reliably
Demeclocycline and lithium both cause nephrogenic DI, but take several days to be effective
Urea causes an osmotic diuresis and enhances water excretion
Na corrected for glucose
Correct na = na + BSL/3
Na deficit equation
Na deficit = 0.6x body wt x (desired na - current na)
Women - 0.5
Causes of SIADH
Neoplastic - SCLC, mesothelioma, sarcoma, leukaemia, lymphoma, pancreas, bladder, prostate
Pulmonary - infection, asthma, CF
CNS - infections, sah, subdue all, CVA, TBI, MS, GBS
Drugs - vasopressin, deamopressin, oxytocin
SSRI, TCA, NSAIDs, opioids, anticonvulsants, PPI, amioderone
Other - post surgical stress response
Adverse effects of hypertonic Saline
Hyperosmolality Overshoot Na CCF and pull oedema Low K NAGMA Phlebitis Coagulopathy Renal failure Reduced LOC rebound increase ICP Seizures Central pontine myelinolysis
Patients at risk of central pontine myelinolysis
Alcoholics Malnourished of Low K Burns Elderly (esp if on thiazides) Liver Tx
symptoms of central pontine myelinolysis
Initially dysarthria and dysphasia
Then confusion, delirium, hallucinations, tremor
Flaccid quadraparesia
Diagnostic requirements of SIADH
Hypotonic hyponatraemia
Urine osmolality > plasma
Urine na >20
Normal renal, hepatic, pituitary, adrenal and thyroid function
Absence of low BP, hypovolaemia, oedema, drugs affecting ADH secretion
Correction by water restriction
Causes of hypotonic hyponatraemia with low urine osmolality and Na
Beer potomania
Psychogenic polydipsia
Excess 5% dextrose
Clinical features of hypernatramia
When Na >155 and osmolality >330mosm/kg
Increased temp Restlessness Irritability Drowsiness Lethargy Confusion Coma
Causes of cranial DI
Idiopathic
Head injury/neurosurgery
Neoplastic - pituitary tumour, hypothalamic mets
Infections - meningitis, encephalitis
Granulomatois disease - sarcoidosis
Vascular - aneurysm, sickle cell anaesmia, Sheehan syndrome
Drugs - ADH suppressed by naloxone, phenytoin
Causes of hypernatraemia
Extrarenal - burns, gastric loss
Salt gain - infusion of bicarbonate, hypertonic saline, ingestion of sea water
Nephrogenic DI - lithium, pyelonephritis, multiple myeloma, amyloid, sarcoidosis
Central DI - TBI, pituitary tumour, meningitis, encephalitis, TB
Renal losses - mannitol, urea, loop diuretics, hyperaldoesteronism
May occur in the recovery phase of an illness as there is more rapid clearance of free water than sodium
Water deficit
Total body water x (1- [ 140/Na] )
Issues needed to be addressed in DI post TBI
Hypernatraemia - give DDAVP if euvolaemic, replace only last hours u/o, avoid fall >0.5/hr
Total body water deficit - replace rapidly if associated with shock, need to use extreme caution - use both isotonic and hypertonic saline to avoid rapid drop
Associated anterior pituitary dysfunction - give hydrocortisone if shocked (will worsen diuresis but improve CVS stability)
Underlying ADH deficiency - DDAVP; selective v2 receptor agonist
Types of DI
Nephrogenic - congenital/acquired
- lithium associated most common
- hypercalcaemia and hypokalaemia also cause
Central - cogential or acquired
Acquired may be transient (inflammation) or permanent (transaction) and absolute or relative
- TBI especially import - seen in up to 70% patients
Gestational - may be associated with HELLP Anand PET
Causes of polydipsia
Psychiatric disorder
Drugs that give sensation of dry mouth eg oxygen, anticholinergics
Hypothalamic lesions that disturb thirst centre
Appropriate detection by osmoreceptors of raised osmolality eg glucose, na, alcohol
How to determine solute diuresis from water diuresis
One off urine osmolality - >300mOsm/kg indicate solute
Commonest cause is glycosuria
Causes of polyuria following head injury
DI CSW appropriate post-resus diuresis Appropriate natriuresis following hypertonic saline Mannitol induced Hypothermic diuresis
Metabolic factors that influence calcium
Protein - calcium increases with decreasing albumin
- often unwell hypoalbuminaemic cancer patients have much higher ca
pH - acidosis -> increased iCa
Phosphate
Mg
Causes of hypercalcaemia
Primary endocrine; PTH increase, thyrotoxicosis, adrenal insufficiency
Paraneoplastic;
- PTH secretion - lung, head and neck, breast, ovarian, bladder
- lytic bone - MM, Breast, harm
- phaeochromocytoma
Granulomatous - sarcoidosis, TB
Drug induced - thiazides, lithium, HRT/oestrogen, TPN
Random causes - immobilisation, rhabdo, milk alkali syndrome
Effects of hypercalcaemia
Polyuria and polydipsia Dyspepsia Depression Muscle weakness Constipation Fatigue Short QT vomiting and diarrhoea Coma Pancreatitis Renal failure (due to vasoconstriction)
Treatment of hypercalcaemia
Fluid +/- frusemide Bisphosphonates Calcitreol Steroids (reduce absorption from gut) Loop diuretics (reduce absorption from renal tubule) NSAIDs
Causes of hypocalcaemia
Citrate Hypoparathyroidism Alkalosis Pancreatitis Tumour lysis Rhabdo - ca may be very low initially, can then become very high Drugs - phenytoin
Instances of hypocalcaemia and acidosis
Acute renal failure Rumour lysis Rhabdo Pancreatitis Ethylene glycol poisoning Hydrofluoric acid poisoning
Clinical manifestations of hypocalcaemia
Cirimoral and peripheral paraesthesia Tetany Seizures Tremor and ataxia Proximal myopathy Hypotension non responsive to unit ropes Long Qt Loss of digitalis effect Apnoea Larygospasm/bronchospasm
Symptoms exacerbated if K and Mg also low
Indications for calcium administration
Symptomatic hypocalcaemia
iCa <0.8n
Hyperkalaemia
Ca channel overdose
Relative indications - Beta blocker od Hypermagnesaemia Hypocalcaemia in the fact of Inotrope requirement MBT
Clinical features of hypokalaemia
Weakness Constipation Ileus Torsades/VT/atrial tachycardia Coma
Prolonged severe hypo can -> rhabdo and nephrogenic DI
ECG changes -
Long PR
TWI
U wave
Aetiology of hypokalaemia
Inadequate diet GI losses Renal losses - - endocrine; conns, cushings, bartters - drugs - diuretics, steroids - RTA - Mg deficiency Compartmental shifts - - alkalosis - insulin - beta adrenergic stimulation - hypothermia - post blood transfusion (delayed) - poisoning - barium, touline
Clinical features of jyperkalaemia
Paraesthesia Weakness Flaccid paralysis Hypotension Bradycardia
ECG - peaked T, flat p, long PR, wide QRS, deep s, sine wave
Aeitiology of hyperkalaemia
Artefactual
Increase from somewhere - transfusion, tissues damage (burns, rhabdo, trauma, tumour lysis)
Decreased renal excretion - renal failure, addisons, drugs (spironolactone. ACEi)
Compartmental shifts -
Acidosis, insulin deficiency, toxins (digoxin, sux)
Causes of hypomagnesaemia
GI disorders - malabsorption, GIT fistula, short bowel, prolonged NG suction, diarrhoea, pancreatitis, parenteral nutrition
Endocrine - hyperparathyroidism, hyperthyroidism, Conns, DM, hyperaldosteronism
Renal disease - RTA, diuretic phase of ATN
Drugs - alcohol, aminoglycosides, amphoteracin B diuretics
Clinical features of hypomagnaesaemia
Physical -
- confusion
- delerium
- tremors
- seizures
- tetany (as with hypo calcaemia)
ECG -
- wide QRS
- peaked T waves (disappear when very severe)
- long PR
Associated biochemical abnormalities -
- Hypokalaemia, refractory to replacement
- hypocalcaemia
- low PTH (in spite of low ca)
- low vit D
Characteristic changes with adrenal insufficicney
low Na high K NAGMA low BSL high Ca
Characteristic changes with hyperaldosteronism
high Na
low K
met alkalosis
Characteristic changes with refeeding syndrome
low K
low PO4
low Mg
low BSL
Characteristic changes with administration of TPN
high BSL
high lipids
NAGMA
Characteristic changes with rhabdo
high K
high PO4
high LDH and CK
myoglobinuria
Characteristic changes with TLS
high PO4 high K high uric acid low Ca HAGMA raised LDH
Characteristic changes with toxic alcohols
HAGMA
High serum osmolar gap
low Ca
Characteristic changes with lithium toxicity
negative anion gap
high Na
Characteristic changes with salycilate toxicity
HAGMA
low K
high urinary K
Causes of hypermagnesaemia
Increased intake - infusion, oral tablets, unregulated absorption (ulcer), milk alkali syndrome
Compartment shift or leak - TLS, rhabdo, acidosis
DEcreased loss - renal failure, primary hyperparathyroidism, lithium therapy, hypoaldosteronism
Clinical features of hyperMg
1.8 - 2 mmol/l - hypocalcaemia, ileus, antiarrhythmic effects
2 - 4mmol/l - hyporeflexia ,muscle weakness, nausea, flushing, headache, lethargy
4 - 6 - resp failure, hypotension, bradycardia, decreased LOC
6 - 10 - apnoe, coma, CHB -> asystole
> 10 - non survivable
Management of hyperMg
usually rapidly corrects with no intervention
can give calcium to antagonise
insulin/dex will promote entry into cells
haemodialysis
HyperPO4 - causes
INcreased inake - TPN, enema
Tissue breakdown - rhabdo, TLS, haemolysis
Decreased excretion - acute or chronic renal failure
Increased tubular reabsorption - hypoparathyroidism, acromegaly, bisphophonates, vit D toxicity
Compartmental shift - carb infusion, hormonal effects (insulin,, glucagon, refeeding), alkalosis
Suprious - hyperlipidaemia, hyperglobulinaemia (MM, waldenstroms), haemolysis
clinical feaures of hypO PO4
neuro - irritablility, hallucination, seizures, coma
CVS - imparied contractility, arrythmias
MSSK - weakness, proximal myopathy, dysphagia, slow vent weaning, rhabdo
Haem - decreased 23DPG (left shift), increased RBC fragility -> haemolysis, thrombocytopaenia
