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3Resuscitationuids
Rapid restoration of circulating volume is vital, particularly for those with
evidence of severe hypovolaemia (Table4.5). Give high- ow O2, establish
IV access, and begin emergency management (E p. 478–9). See Box4.6.
Fluid challenge This implies rapid delivery of a bolus of uid with monitoring
for eects to guide further uid management. Abolus of 500mL crystalloid,
eg 0.9% saline IV (250mL if frail or heart problems, 20mL/ kg in children), is
infused over <5min. Reassess immediately: if evidence of hypovolaemia
persists, consider further 250– 500mL uid boluses. Large volumes may
eventually be needed, but seek senior help and involve ICUearly.
T Box 4.6 Choice ofuid inresuscitation
Choice of synthetic resuscitation uid has historically split into a debate between
the use of crystalloids (aqueous solutions of mineral salts) and colloids (containing larger, insoluble molecules). Although colloids might theoretically exert an
osmotic load keeping more uid in the circulation, this eect may be overstated
and must be set against the higher cost of colloids. Trial data have rmly come
down in favour of the use of crystalloids, with evidence of increased rates of
renal failure
6
and death7 associated with colloid resuscitation. Evidence for choice
of crystalloid is less robust, and both 0.9% saline and physiological salt solutions
represent reasonable choices. Of course, blood represents a highly physiological
replacement uid when used in haemorrhage, but is rarely a practical or necessary choice in other settings. Human albumin solutions should oer the same
osmotic benets as proposed for colloids, but in ICU study data any survival
advantage appears small and limited to patients with severe sepsis.
8
Maintenanceuids
$ Prescribing ‘routine’ uids is a common task for Foundation doctors, and
one your seniors are unlikely to take much interest in until you make a mistake.
When asked to prescribe uids, always consider why a patient is on uids, what
their electrolyte needs are (look at recent blood results), and whether further
uids should be given (think of replacement for insensible losses, eg fever). If in
any doubt, assess the patient for RR, JVP, and basal lung crepitations.
Maintenance requirements Typically adults require 25– 30mL of water/ kg/
24h to cover their urine output and insensible losses (sweat, respiration,
stool). This equals to about 2– 2.5L per day for a 70– 80kg adult.
9
Several
additional sources of uid losses may occur in acutely ill patients:
RecordablePolyuria, NG aspirate, diarrhoea, vomiting, drains.
InsensibleWound leakage, pyrexia, tachypnoea,burns.
Third space(E p. 402), eg pancreatitis, post- op.
As much as possible, intake should come through the GI tract— always
maximize PO intake (you can prescribe water, eg 250mL QDS). Consider
using NG uids as an alternative to IV where inadequate PO intake
persists ≥3d. Alternatively, for an elderly patient managing insucient
volumes PO and who has no need for an IV cannula, L 0.9% saline SC
overnight (2h) may be all that is required. Always explore with seniors
which patients need to remainNBM.
6
Myburgh JA, etal. NEJM 202;367:90 available free at Mnejm.org/doi/0.056/NEJMoa209759
7
Perner A, etal. NEJM 202;367:24 available free at Mnejm.org/doi/full/0.056/NEJMoa204242
8
SAFE Study Investigators NEJM 2004;350:2247 available free at Mnejm.org/doi/0.056/NEJMoa040232
9
Paediatric uid requirements are on Ep. 405.
403IVFLUIDS
404 CHAPTER4 Fluids andrenal
Estimating uid requirements24h requirements can best be estimated from
review of an accurate uid balance chart. This is especially useful in patients at risk of uid overload. Three components need to be considered:
• Recorded losses over last 24h (from uidchart)
• Estimate of insensible losses (usually 0.5– .5L/ 24h)
• Estimate of uid decit (from history, examination, obs, and uid chart).
Where a uid balance chart is not available, estimate needsas:
• Estimate of maintenance requirement from weight (25– 30mL/ kg/ 24h)
• Additional uids if signicant insensible losses are expected (0.5– .5L/ 24h)
• Estimate of uid decit (from history, examination,obs).
Beware groups of patients who may need less uids than estimated:elderly/ frail, low BMI, heart problems, CKD, partial oral intake.
Electrolyte and glucose requirementsEstimation of electrolyte requirements
should take into account current U+E, medications (especially diuretics
and supplements), and uid loss. Fluid loss from stomas or vomiting is
electrolyte-rich. Basic maintenance requirementsare:
+
•
Na
, K+, Cl− mmol/ kg/ 24h— eg typically 60– 80mmoladay
•
Glucose 50– 00g/ 24h— 5% glucose contains 5g/ 00mL.
Table 4.6 shows the electrolyte content of some commonly used IV
uids. Due to the potential to trigger dysrhythmias, the
of potassium administration outside of HDU/ ICU is 0mmol/ h
PrescribingHaving decided the 24h uid and electrolyte requirement, con-
vert total needs into suitable 500– 000mL bags to run at appropriate
rates. If there is any decit, the initial bags should be run more quickly to
correct hypovolaemia. Where safe, prescribe the uids so that they run
out during the normal working day to reduce work for those on call.
Table4.6 Composition ofcommon IVuids
Content Plasma 0.9%
Na+ (mmol/L) 35–45 54 3 0 3
–
(mmol/L) 95–05 54 0 3
Cl
+
(mmol/ L) 3.5–5.3 0 5 0 0
K
–
HCO
3
(mmol/ L)
+
Ca
(mmol/ L)
24–32 0 29 (lactate) 0 0
2.2–2.6 0 2 0 0
Mg+ (mmol/ L) 0.8–.2 0 0 0 0
Glucose
(mmol/ L)
3.5–5.5 0 0 278 (50g) 222 (40g)
pH 7.35–7.45 4.5–7.0 5–7 3.5–5.5 4.5
Osmolarity
(mOsm/ L)
Table adapted from Mhttps://www.nice.org.uk/guidance/cg74
‡
L 0.9% saline/ 24h already exceeds daily Na+ requirements. Large volume saline infusions result
in hyperchloraemic metabolic acidosis and potential overload of renal sodium excretion capacity.
*Glucose has 2 stereoisomers. The D- isomer is known as dextrose, which is the form found in
infusion uids. In practical usage, ‘dextrose’ and ‘glucose’ are interchangeable, since alternative
isomers of glucose are not prescribable, although can be a source of some confusion.
275–295 308 278 278 284
Hartmann’s 5%
‡
NaCl
dextrose
maximal safe rate
0.8%NaCl/
4% dextrose
*
.
*
Specialcases
Post- opPatients may leave surgery with hypovolaemia due to blood loss
and third- space loss; they may require more uids to make up this deficit. Despite lysis of cells during surgery causing a release of K+, most
postoperative patients who remain NBM will still require supplementary
KCl in their postoperative uid replacement after24h.
Intestinal uid losses Most intestinal uids have a composition similar to
0.9% saline with 20mmol/ L of KCl and should be replaced with this. For
the exact composition of dierent intestinal uids check theBNF.
Heart failurePatients with previous heart disease are more prone to uid
overload and pulmonary oedema. Simple attention to uid balance prevents problems in the majority of patients. If uid overload develops, the
patient may require a dNa+ diet, daily weights, and uid restriction (eg
.5L/ 24h). There is no logic to the routine prescribing of furosemide
alongside maintenance uids.
Chronic liver failure Excess Na
+
may cause ascites. Restrict Na+ by using
5% glucose; .5L/ 24h uid restriction is sometimes required. If uid resuscitation is required use salt- poor albumin (a blood product, see BNF).
Recheck U+E regularly to ensure not becoming hyponatraemic.
Acute kidney injury
Ensure adequate and timely administration of crystalloids to correct for any hypovolaemia. Avoid additional K+ unless hypokalaemic. Further IV uids should be determined by uid balance ±CVP
in HDU/ ICU, along with regular repeatU+E.
Chronic kidney disease A reduction in glomerular ltration rate (GFR)
means that the kidney cannot excrete as much water, Na+, or K+. In mild
CKD excess uids and Na+ should be avoided, though acute deterioration in renal function is usually a sign of hypovolaemia. In severe CKD,
restriction of Na+, K+, and uid (eg .5L/ 24h) is required.
If in doubt Reassess and seek senior advice. Fluid prescribing is
3
complex, the condition of your patient will change, and there is no substitute for reassessing prior to prescribing the next bag of anyuid.
Children’s maintenanceuids
0
Milk volumeBabies >5d require 50mL/ kg milk eachday.
Maintenance Calculate uid requirements (Table4.7). Isotonic crystalloids
with a sodium content of 3–54mmol/L are the initial choice for the rst
24h, subsequent prescriptions should be guided by plasma electrolytes.
Example
23kg child:(0 × 00mL) + (0 × 50mL) + (3 × 20mL)=560mL/ 24h.
405IVFLUIDS
Table4.7 Maintenance uids inchildren
Weight Fluids/ kg/ 24h Fluids/ kg/ h Expected 24h volume
First 0kg 00mL/ kg/ 24h 4mL/ kg/ h 0– 000mL
0– 20kg 50mL/ kg/ 24h 2mL/ kg/ h 000– 500mL
Above 20kg 20mL/ kg/ 24h mL/ kg/ h 500– 3000mL
0
NICE guidelines for IV uid prescribing for children can be found at Mnice.org.uk/guidance/ng29
Children are especially prone to iatrogenic electrolyte disturbances, especially hypo- and
hypernatraemia, both of which can be fatal. Therefore, uid choice requires specialist advice.
406 CHAPTER4 Fluids andrenal
2Potassium emergencies
2 Airway
2 Breathing
2 Circulation
Check airway is patent; consider manoeuvres/ adjuncts
If no respiratory eort—
If no palpable pulse—
CALL ARREST TEAM
CALL ARREST TEAM
3Call for senior help early if patient deteriorating. See Box 4.7.
Hypokalaemia
(K+ <2.5mmol/ L or <3mmol/ L with ECG changes.)
•
ECG changes Arrhythmias, prolonged PR interval, ST depression,
small/ inverted T waves, U waves (after Twave)
•
5L/ min O
•
Monitor debrillator ECG leads, BP, pulse oximeter
•
Venous access, take bloods for urgent repeat U+E,Mg
•
Replace K
•
•
• Look for
•
Call for seniorhelp
if SOB or sats<94%
2
2+
+
, 40mmol/ L KCl in L 0.9% saline IV unless oliguric:
, VBG
do not replace K+ faster than 0mmol/ h outside of HDU/ ICU
never give KClSTAT
cause Ep. 407
• Reassess, starting with A, B, C…
Hyperkalaemia
(K+ ≥6.5mmol/ L or >5.5mmol/ L with ECG changes.)
2
• ECG changes Arrhythmias, at P waves, wide QRS, tall/ tented Twaves
•
5L/ min O
•
Monitor debrillator ECG leads, BP, pulse oximeter
•
Venous access, take bloods for urgent repeatU+E and VBG
• If ECG changes seen or K
•
•
•
in all patients
2
+
≥6.5mmol/ L (arrhythmias Ep. 262):
30ml of 10% calcium gluconate IV given over 5–10min,3 repeat
dose after 10mins if ECG changes persist
0units Actrapid® in 25mL of 20% glucose over0min
salbutamol 5mg nebulizer, repeat up to 0–20mg
• Consider potassium binders, eg sodium zirconium cyclosilicate,
patiromer
• Call for seniorhelp
• Reassess, starting with A, B, C
• Check K
+
at 4h and glucose at regular intervals for 2h for rebound
hyperkalaemia or hypoglycaemia.
4
2Box 4.7 Life- threateningcauses
Hyperkalaemia
• Renal failure
• Acidosis
Hypokalaemia
• Hypovolaemia
• Alkalosis.
• Tissue necrosis
2
Renal Association clinical practice guidelines for treatment of acute hyperkalaemia can be found
at Mhttps://ukkidney.org/
3
Calcium gluconate should be given more slowly in patients on digoxin—over 20–30min.
4
Patients with blood glucose 4–7mmol/L pre-treatment are at risk of hypoglycaemia post treat-
ment and may require 0% glucose infusion at 50–00mL/h for 5h.
Electrolyte imbalance
3Hypokalaemia (K+ <3.5mmol/ L.)
2Worrying features dGCS, chest pain, palpitations, abnormalECG.
CausesVomiting, diarrhoea, most diuretics, steroids, and Cushing’s, inad-
equate replacement in uids, alkalosis, Conn’s syndrome.
SymptomsWeakness, cramps, palpitations, nausea, paraesthesia.
SignsMuscle weakness, hypotonia, arrhythmias.
Investigations blds Recheck U+E looking for coexisting electrolyte
imbalances, in particular dMg
attening or inversion, U waves, ST depression, atrial arrhythmias.
TreatmentIf K
to IV uids or give Sando- K
writing up Sando- K
+
≥2.5mmol/ L with no ECG changes add 20– 40mmol KCl
®
treatment. Replace any concurrent dMg
0.9% saline IV over h). If K
plan Ep. 406. Stop any causative medications.
3
Hyperkalaemia (K
2Worrying features dGCS, chest pain, palpitations, abnormalECG.
CausesHaemolysed samples (likely if several hours taken to reach lab),
AKI, CKD, K
+
- sparing diuretics (spironolactone, epleronone, amiloride),
ACEi, trauma, burns, iatrogenic, rhabdomyolysis, tumour lysis
syndrome, large blood transfusions, Addison’s disease. See Box 4.8.
SymptomsPalpitations, dizziness, chestpain.
SignsAssess haemodynamic stability, irregular pulse, stigmata ofCKD.
Investigations blds Urgent repeat U+E; if K
ECG changes or the sample is reported as haemolysed then await the
repeat sample, otherwise follow the treatment plan (E p. 406); if on digoxin, check levels since digoxin toxicity will worsen hyperkalaemia;
For acidosis if AKI; ECG Initially peaked T waves, later broad QRS
ABG
and at Pwaves, ultimatelyVF.
TreatmentCa
insulin move K
2+
gluconate protects the heart against iK+. Salbutamol and
+
into cells to reduce plasma levels in the short term (– 2h)
after which a rebound increase may occur. Furosemide (with IV uids if
necessary) or calcium polystyrene sulfonate (takes 24h, give with lactulose
30mL/ 6h PO) enhance K
be necessary (E p. 395). Stop any causative or nephrotoxic medication.
2+
;ABGIf alkalosis suspected;ECG T-wave
®
2 tablets/ 8h PO and monitor U+E; consider
only for 3– 5d to prevent continuous unmonitored
+
<2.5mmol/ L or ECG changes, see treatment
+
>5.5mmol/ L.)
2+
(eg 8mmol MgSO4 in 00mL
+
<6.5mmol/ L with no new
VBG/
+
excretion. If refractory or acidotic, dialysis may
407ELECTROLYTE IMBALANCE
T Box 4.8 Spurious hyperkalaemia
Serum potassium levels may be artefactually high due to haemolysis (difcult venepuncture, shaking of the tube); EDTA contamination (FBC
bottle taken before U+Es); delay in processing (more pronounced in
cold temperatures); erythrocytosis, leucocytosis, or thrombocythaemia.
408 CHAPTER4 Fluids andrenal
Hyponatraemia(Na
+
<33mmol/ L.)
2Worrying features dGCS, irritable, seizures, iHR,dBP.
Ask about Diarrhoea, vomiting, abdo pain, tiredness, urine frequency,
quantity and colour, thirst, constipation, SOB, cough, chest pain, weakness, head trauma;
PMHHeart, liver, or kidney disease;DHDiuretics, opi-
oids, antipsychotics, amiodarone, proton pump inhibitors, SSRIs, IV uids.
Look forAssess uid balance and volume status (E p. 402), basal creps,
oedema (legs and sacrum), ascites, focal neurology, conscious level (if
+
Na
<20mmol/ L the patient may become irritable or confused; if
<0mmol/ L there may be seizures orcoma).
Investigations blds FBC, U+E, LFT, CRP, plasma osmolality;Urine Send
paired sample for osmolality and Na
+
; assess underlying cause as in
Table4.8 (also see Box4.0).
Spurious dNa+ (pseudohyponatraemia) Blood from drip arm, hyperlipid-
aemia, hyperglycaemia. Discuss with lab if unsure.
Table4.8 Assessing hyponatraemia
Fluid
status
Urine Na
(mmol/L)
Causes Diuretics,
Hypovolaemic Euvolaemic Hypervolaemic
+
>20 <20 Usually >20 >20 <20
Addison’s,
salt-losing
renal disease,
cerebral salt
wasting
Vomiting/
diarrhoea,
third spacing
(burns,
pancreatitis,
trauma)
SIADH,
Addison’s,
diuretics/ACEi,
hypo-
thyroidism
Acute-onchronic
renal
failure,
pregnancy
Nephrotic
syndrome,
cirrhosis,
CCF
K Box 4.9 Syndrome ofinappropriate ADH secretion
(SIADH)
In this condition, inappropriate hypothalamic release of ADH leads to
euvolaemic hyponatraemia. Beware of overcalling this diagnosis, which
requires a careful workup:
• Concentrated urine despite dilute plasma (ie urine osmolality
>plasma): generally plasma osmolality <275mOsmol/ kg and urine
osmolality >500mOsmol/ kg
• Normal adrenal and thyroid function (check TSH and short
Synacthen
®
test)
• No recent diuretics
• Clinical euvolaemia
• Urine sodium >20mmol/ L.
Causes include malignancy (lung, pancreas, lymphoma), lung infections,
CNS infections or vascular events, drugs (eg SSRIs, tricyclics, carbamazepine, antipsychotics), or idiopathic. Management requires uid restriction
(initially L/ 24h) ±ADH antagonists (eg demeclocycline 300mg/ 2hPO).
TreatmentAlthough acute hyponatraemia (<48h duration) can be rapidly
corrected, chronic hyponatraemia (or where the time course is unclear)
should be corrected slowly to prevent uid overload or osmotic demyelination. Aim for a rise of no more than 0mmol/ L/ 24h. Get senior help
if seizures or coma (the rare situation where it may be necessary to raise
+
Na
rapidly by 75mmol/ L using hypertonic saline) or if Na+ <20mmol/
L. In all patients monitor uid balance closely with catheter, regular obs,
and possibly CVP. Repeat U+E daily, or more frequently if neurological
signs. Assess cause using Table4.8 and treat accordingly.
•
Hypovolaemic Replace lost uid with 0.9% saline according to degree of
dehydration (E p. 404); severe hypovolaemia should be corrected
(Ep. 482) and takes precedence over hyponatraemia. Try to establish
the cause of uid loss and treat accordingly. Stop diuretics
•
Normovolaemic or mild overload Slow 0.9% saline IV eg L/ 8– 0h, Na
+
levels should rise over a few days. If urine osmolality >500mOsmol/ kg
consider SIADH and restrict uids (Box4.9)
•
Oedematous Urine Na
+
usually <0mmol/ L, identify and treat the
underlying cause (see relevant chapter).
I Box 4.0 Causes ofhyponatraemia covered
elsewhere
Heart failure E p. 282 Renal failure E p. 395
Liver failure E pp. 327–31 Nephrotic syndrome E p. 398
Hypernatraemia(Na
+
>46mmol/ L.)
2Worrying features dGCS, iHR,dBP.
CausesFluid loss (diarrhoea, burns, fever, glycosuria, eg DM, diabetes in-
sipidus) or inadequate intake (impaired thirst response in elderly or hypothalamic disease); more rarely excess Na
+
(iatrogenic, Conn’s syndrome).
SymptomsAnorexia, nausea, weakness, hyperreexia, confusion,dGCS.
SignsAssess uid balance, volume status (E p. 402), neurological decit.
Investigations bldsPlasma osmolality (likely to be raised);UrineOsmolality
(>400mOsmol/ kg if uid loss, <400mOsmol/ kg if excess Na
betes insipidus, normal range 350– 000mOsmol/ kg); consider
or
MRIif suspect centralcause.
+
, or in dia-
CThead
Treatment $ Cells rapidly adapt to raised osmolality of extracellular uid
by retention and production of intracellular osmolytes. This prevents osmotic uid losses from inside the cell, but if extracellular Na
+
concen-
tration rapidly corrected, osmotic forces will now drive uid into cells,
causing lysis resulting in neurological damage anddeath.
Hence aim for slow correction of Na
most). Treatment is guided by volume status:
•
Hypovolaemic Give 0.9% saline L/ 6h (prevents sudden Na
+
(0mmol/ L/ 24h at the very
+
shifts) until
normovolaemic
•
Normovolaemic Encourage oral uids or 5% glucose L/ 6h. Monitor uid
balance and plasma Na
+
; consider a urinary catheter.
409ELECTROLYTE IMBALANCE
410 CHAPTER4 Fluids andrenal
Hypocalcaemia(Corrected Ca
2+
<2.2mmol/ L.)
$ Although >99% calcium is stored in bones, and most of the re-
mainder is intracellular, extracellular calcium is critical for neuromuscular and cardiac function. Albumin binds around 40% of extracellular
calcium, so hypoalbuminaemia may give falsely low recordings of serum
calcium; always check the ‘corrected calcium’. Gut, renal, and bone calcium handling is critically regulated by vitamin D, which requires hydroxylation in functioning kidneys and liver to be active, and byPTH.
2Worrying features dGCS, chest pain, palpitations, dBP, abnormalECG.
Causes Vitamin D deciency (elderly, Asians, Africans, CKD, intestinal
malabsorption, eg coeliac, Crohn’s), hypoparathyroid, acute pancreatitis, alkalosis, dMg
2+
, alcoholism.
SymptomsSpasm of hands and feet (carpopedal), twitching muscles, tin-
gling around the mouth, fatigue, depression, dry skin, coarsehair.
Signs Hyperreexia, tetany, Trousseau’s (spasm of hand from inated
BP cu ) and Chvostek’s (unilateral twitching of face from tapping facial
nerve 2cm anterior to auditory meatus), dBP, bradycardia, arrhythmias.
Investigations BldsU+E, Ca
ECGProlonged QT, ST abnormalities, arrhythmias.
Treatment Treat arrhythmias according to E p. 262. If tetany is severe
give 0mL 0% Ca
correct coexistent dMg
tomatic, monitor. Prolonged dCa
2+
Ca
supplements, eg Calcichew- D3 Forte® one tablet/ 24hPO.
ComplicationsArrhythmias, seizures, cataracts, bone fractures.
Primary hypoparathyroidism dPTH, despitedCa
CausesIatrogenic (neck surgery, irradiation), autoimmune, metal overload.
Investigations dCa
TreatmentVitamin D, eg calciferol – 2.5mg/ 24hPO.
2+
3−
, PO
, Mg2+, albumin, ALP, PTH, vitamin D;
4
2+
gluconate IV over 0min. Always assess for and
2+
. If Ca2+ decit is mild and the patient is asymp-
2+
will need vitamin D replacement and
2+
.
2+
, dPTH, iPO
3−
.
4
PseudohypoparathyroidismGenetic resistance to PTH, presents with dCa
but high PTH and dysmorphic features (short stature, strabismus, short
4/ 5th metacarpals, low IQ, obesity);
5
treat as hypoparathyroid.
Rickets/ osteomalacia Rickets is the childhood equivalent of osteomalacia,
both characterized by vitamin D deciency or defect in metabolism.
•
Features dCa
spontaneous fractures (eg of ribs), rickets rosary (prominent
2+
, dPO
3−
, iALP, decreased urine Ca2+, crush fractures,
4
costochondral junctions), long bone bowing and Looser’s zones
(pseudofractures, perpendicular to cortex, common in femoral/
humeral necks) onX- ray
•
Treatment This depends on cause, but usually simply by intake of adequate
diet (egg yolk, milk, some fortied cereals); may require calciferol and Ca
supplements (eg Calcichew- D
Forte® one tablet/ 24hPO).
3
2+
2+
5
Patients with the morphological appearance of pseudohypoparathyroidism but normal Ca2+ and
PTH, are said to have
pseudopseudohypoparathyroidism.
411ELECTROLYTE IMBALANCE
Hypercalcaemia(Corrected Ca
2+
>2.6mmol/ L.)
2Worrying features dGCS, chest pain, palpitations, iHR, dBP, abnormalECG.
Causes Primary/ tertiary hyperparathyroidism, malignancy (myeloma,
bone metastases, PTH- related peptide secreting tumours), excess
vitamin D supplements, sarcoidosis.
Symptoms Bones (bone pain ±fractures), Stones (renal),Moans (depres-
sion),
Groans (abdo pain). Also vomiting, constipation, weakness, tired-
ness, thirst, polyuria, weightloss.
SignsHypertension, arrhythmias, dehydrated (shock if severe), cachexia,
bony tenderness secondary to a local lesion— especially alongspine.
Investigations bldsFBC, U+E, Mg
for PTH (may have to be on ice— discuss with lab); consider ESR, serum
and urine electrophoresis;
2+
, Ca2+, PO
3−
, ALP; send paired sample
4
ECGShort QT, arrhythmias; CXR; Bone scan.
Treatment This depends upon IV uids to correct any volume decit, then
further uid rehydration with coadministration of 40mg/ 2h PO or IV
furosemide; consider catheterization and CVP monitoring to assess uid
balance; monitor U+E, Ca
2+
, and Mg2+ daily. IV bisphosphonates (eg
pamidronate 30mg in 300mL 0.9% saline over 3h) are useful in refractory hypercalcaemia. Investigate and treat thecause.
Complications AKI, arrhythmias, osteopenia, renal stones, peptic ulcers,
pancreatitis.
Primary hyperparathyroidism iPTH from parathyroid tumour; Investi gations
iPTH, iCa
Secondary hyperparathyroidism iPTH caused by dCa
cause of dCa
2+
, iALP, dPO
2+
(Ep. 410).
3−
;TreatmentCorrect iCa2+ then parathyroidectomy.
4
2+
; treat the underlying
Tertiary hyperparathyroidismSame presentation and treatment as primary,
but caused by a parathyroid adenoma due to prolonged secondary
hyperparathyroidism. Seen in end- stage renal failure.
Myeloma $ Plasma- cell malignancy secreting monoclonal immunoglobu-
lins. Presentations include asymptomatic hypercalcaemia, renal failure,
bleeding, infection, or fracture.
Investigations iESR, iCa
2+
, normal ALP, often a degree of renal impairment,
monoclonal immunoglobulin band in urine or plasma (>30g/ L, or >0%
plasma cells on bone marrow biopsy else MGUS E p. 48);
2+
iCa
as above and with pamidronate IV; give adequate analgesia. Attempted
TreatmentCorrect
cure requires bone marrow transplant. Lesions can be treated palliatively with
radiotherapy or chemotherapy;
Complications Infection, CKD, haemorrhage.
Paget’s disease $ Excess bone remodelling leads to structurally disor-
ganized and weakened bone prone to fracture and deformity. Typically
found in axial bones of elderly.
Features iALP, Ca
lesions, and coarse trabeculations on X- ray;
bisphosphonates, surgery for fractures and nerve entrapment;
tions
Fractures, osteoarthritis, osteosarcoma (rare), cranial nerve com-
2+
normal (but may be raised if immobile), lytic
Treatment Analgesia,
Complica-
pression (eg new deafness), high-output heart failure.
Bone mets
Five cancers commonly metastasize to bone. These can be remem-
bered as ‘BLT with Kosher Pickle’:Breast Lung Thyroid Kidney Prostate.
