Oxford Handbook of Critical Care - part 8 ppsx

See also: Venti latory support—indicati ons, p4; Conti nuous positi ve airway pressure, p26; Non-invasi ve respiratory support, p32; Acute respiratory distress syndrome 1, p292; Acute re

P.402

possibly, a decreased li fespan

Rarer causes include:

Microcyti c anaemia—predominantly iron defi ci encyNormocyti c

Chroni c diseaseBone marrow fail ure (i di opathi c, drugs, neopl asm, radi ati on)Haemolysis

Renal fail ureMacrocyti c—vitamin B12 and folate defici ency, alcoholi sm, ci rrhosi s, si derobl astic anaemi a, hypothyroidi smCongeni tal di seases—sickle cel l, thalassaemi a

Management

Treatment of the cause where possi ble

1

Blood transfusi on:

The i deal haemogl obi n l evel for optimal oxygen carriage and vi scosity remains contentious A recentmulticentre tri al showed improved outcomes if a trigger of 7 g/dl was used A hi gher transfusi on threshol d,e.g 9–10 g/dl , may be needed in those with cardiorespiratory disease

Transfusion i s usuall y gi ven as packed cell s with or wi thout a smal l dose of furosemi de to maintai n fluidbalance This may need to be given rapidl y duri ng active bl ood loss, or sl owl y for correcti on of a graduall yfall ing haemoglobin level

Rarel y, patients admitted wi th a chronicall y l ow haemogl obin, e.g <4–5 g/dl, which often fol lows l ong termmalnutriti on or vi tami n defi ci ency, wil l need a much sl ower elevati on in haemoglobin level to avoid

precipi tating acute heart fail ure An i nitial target of 7–8 g/dl i s often acceptable Obvi ously, this may need

to be al tered in the l ight of any concurrent acute i llness where el evation of oxygen deli very i s deemednecessary

Erythropoeiti n reduces the need for blood transfusion i n l ong-term ICU patients and may be useful in those

wi th multi ple antibodi es or decli ning transfusi on for rel igious reasons

2

Key trial

Hebert PC, et al for the Transfusi on Requirements in Criti cal Care Investigators, Canadi an Cri ti cal Care Tri alsGroup A mul ticenter, randomized, control led cl ini cal trial of transfusi on requirements in critical care N Engl JMed 1999; 340:409–17

Sickle cell disease

A chroni c, heredi tary disease al most enti rel y confined to the black population where the gene for Hb S is i nherited

from each parent The red bl ood cell s l ack Hb A; when deprived of oxygen these cell s assume si ckl e and other bizarre

shapes resul ti ng in erythrostasi s, occlusion of blood vessels, thrombosis and tissue infarcti on After stasi s, cells

rel eased back i nto the circul ati on are more fragil e and prone to haemolysis Occasi onally, there may be bone marrow

fai lure

Chronic features

Patients with sickle cell disease are chroni cal ly anaemi c (7–8 g/dl) wi th a hyperdynami c circul ati on Splenomegal y i s

common in youth but, with progressive episodes of i nfarction, spleni c atrophy occurs l eading to an increased risk of

infection, particularl y pneumococcal

Chroni c features i nclude skin ul cers, renal fai lure, avascular bone necrosis (± superveni ng osteomyel iti s, especial ly

Salmonella), hepatomegaly, jaundice and cardiomyopathy Sudden cardiac death is not uncommon, usuall y before the

age of 30

Sickle cell crises

Cri ses are precipitated by various tri ggers, e.g hypoxaemi a (air travel, anaesthesia, etc.), i nfecti on, cold,

dehydrati on and emoti onal stress

Thrombotic crisis

Occurs most frequently in bones or joi nts but also affects chest and abdomen givi ng rise to severe pai n Neurol ogi cal

symptoms (e.g sei zures, focal si gns), haematuri a or priapism may be present Pul monary crises are the commonest

P.404

reason for ICU admi ssion; secondary chest infection or ARDS may supervene, worseni ng hypoxaemi a and further

exacerbating the cri sis

Prophylaxis against cri ses incl udes avoidance of hypoxaemia and other known preci pitati ng factors, prophylacti c

penici ll in and pneumococcal vaccine, and exchange transfusi ons

Painful crises usuall y require prompt opi ate infusions Although psychological dependence i s high, anal gesiashould not be wi thheld

Oxygen therapy, p2; Pulse oximetry, p90; Full blood count, p154; Bacteriology, p158; Acute chest i nfection (1),

p288; Acute chest infection (2), p290; Acute renal fail ure—diagnosis, p332; Acute renal fai lure—management, p334;

Jaundi ce, p358; Anaemi a, p400; Haemol ysi s, p404

Haemolysis

Shorteni ng of erythrocyte l ifespan bel ow the expected 120 days Marked intravascul ar haemol ysi s may lead to

jaundi ce and haemoglobinuri a

Causes

Blood transfusi on reacti onsHaemolytic uraemic syndrome (mi croangiopathic haemol yti c anaemia)Trauma (cardi ac val ve prosthesi s)

Malari aSickle cell haemol yti c cri sisDrugs—e.g high-dose peni ci lli n, methyl dopaAutoimmune (cold- or warm antibody-mediated)—may be i diopathic or secondary, e.g l ymphoma, SLE,mycoplasma

Glucose-6-phosphate dehydrogenase defi ci ency—oxidati ve cri ses occur foll owi ng ingestion of fava beans,pri maquine, sul phonamides l eading to rapid onset anaemi a and jaundi ce

RBC fragmentation (microangi opathi c haemolytic anaemia)Coombs' test (immune-mediated haemolysis)

Ful l blood count, p154; Blood transfusi on, p182; Acute renal fai lure—diagnosis, p332; Acute renal

fai lure—management, p334; Jaundice, p358; Anaemia, p400; Sickle cel l disease, p402; Pl atelet di sorders, p406;

Mal ari a, p490; Vascul itides, p494; HELLP syndrome, p540

Platelet disorders

Thrombocytopenia

Rarely symptomatic until the platel et count <50 × 109/l ; spontaneous bl eeding is more li kel y <20 × 109/l Al though

bleedi ng is often minor, e.g ski n petechi ae, oozing at i ntravascular catheter sites, it may be massi ve or

li fe-threateni ng, e.g haemoptysi s, intracranial haemorrhage

Spl enomegalyThromboti c thrombocytopenic purpura (TTP), haemol yti c uraemic syndrome (HUS)Idi opathi c thrombocytopenic purpura (ITP)

Specific infections, e.g measles, i nfecti ous mononucl eosis, typhusColl agen vascular diseases, e.g SLE

2

Unl ess actively bl eeding, avoi d platelet transfusions in TTP or HUS

3

Deranged platelet function

Functi on may be deranged, al bei t with normal counts, e.g fol lowing aspi rin wi thi n past 1–2 weeks, epoprostenol ,

uraemi a Fresh platel ets may be required i f the patient i s symptomati c In uraemi a, one dose of vasopressi n (20µg IV

over 30 min) may be useful before surgery

Thrombocythaemia

Rare i n ICU patients; pl atelet counts often exceed 800 × 109/l

As the major ri sk is thrombosis, management i s based upon mobil ising the pati ent and administration of either

prophylacti c aspi ri n (150 mg bd PO) or LMW heparin (5000 IU od SC) Di pyridamole (300–600 mg tds PO) is

occasi onall y used

See also:

Plasma exchange, p68; Ful l blood count, p154; Bl ood transfusion, p182; Anticoagul ants, p248; Blood products, p252;

Intracranial haemorrhage, p376; Abdominal sepsis, p350; Bl eedi ng di sorders, p396; Haemolysis, p404; Systemic

inflammation/multi organ fai lure, p484; Vascul iti des, p494

Neutropenia

Neutropenia is defined as a neutrophil count <2 × 109/l Li fe threateni ng infections may develop below 1 ×109/l and

more commonl y below 0.5 × 109/l Absolute numbers of neutrophils are more relevant than percentages as the total

whi te cel l count may be either decreased, normal or increased

Haemopoietic di seases, e.g leukaemia, l ymphoma, myel oma or as a consequence of chemotherapy or radi ationNutritional defici encies, e.g folate, vitami n B12, mal nutrition

Adverse drug reaction, e.g carbi mazole, sulphonami desPart of aplasti c anaemia, e.g idi opathi c, drugs, i nfecti onSpecific infections, e.g brucel losis, typhoid, vi ral , protozoalHypersplenism

Antineutrophil antibodi es, e.g systemic lupus erythematosi s

Infections

Ini tial i nfecti ons are with common organisms such as pneumococci, staphylococci and col iforms

With recurrent infections or after repeated courses of antibiotics, more unusual and/or anti biotic-resi stant

organi sms may be responsi bl e, e.g pseudomonas, fungi (particularl y Candida and Aspergillusspp.),

Have a high index of suspi cion for atypical infections such as fungi

Although prophyl actic broad-spectrum antibiotics are often prescribed, thi s encourages antibiotic

7

P.410

P.411

resi stance Another al ternative i s to maintai n stri ct infection control wi th regul ar survei ll ance and to treat

i nfecti ons aggressi vel y as i ndi cated by li kel y sites and lab resul ts Avoi d uncooked foods, e.g sal ads(pseudomonas risk) and bottled pepper (aspergil lus)

Granul ocyte-col ony stimulating factor (G-CSF) is frequentl y given to sti mul ate a bone marrow response

Ful l blood count, p154; Bacteriol ogy, p158; Anti microbial s, p260; Infecti on control—general princi ples, p476;

Infection—di agnosis, p480; Infection—treatment, p482

Leukaemia

Such pati ents may present acutel y to an ICU wi th compl ications ari si ng from ei ther the di sease or the therapy

Complications arising from the disease

Decreased resistance to infectionHypervi scosi ty syndrome—drowsi ness, coma, focal neurol ogi cal defectsCentral nervous system invol vement

Anaemi a, thrombocytopenia, bleeding tendency, DIC

Complications arising from the therapy

Tumour lysis syndrome—hyperkal aemi a, hyperuri caemia and acute renal fail ure may follow rapi d destructi on of alarge whi te cel l mass

Neutropeni a and immune compromi se with an i ncreased risk of i nfecti onAnaemi a

Thrombocytopenia leadi ng to spontaneous bleedi ng, usual ly from i ntravascular catheter sites, ski n, lung, gut andbrain

Lung fi brosi s, e.g foll owi ng radiotherapy, bleomycinMyocardial fail ure, e.g fol lowing mi tozantrone

Graft versus host disease (GVHD)—features include mucositis, hepatitis, jaundice, diarrhoea, abdominal pain,rash and pneumoniti s

Management

Tumour lysis syndrome can be prevented by adequate hydrati on, mai ntaining a good di uresi s and admi ni steringall opurinol Once establ ished, haemo(di a)filtration and other measures to l ower serum potassi um levels may benecessary

Platel et transfusi ons are required i f counts remai n <10–20 × 109/l, or if <50 × 109/l and remaining symptomatic

or undergoing an i nvasive procedure

See also:

Venti latory support—indicati ons, p4; Conti nuous positi ve airway pressure, p26; Non-invasi ve respiratory support,

p32; Acute respiratory distress syndrome (1), p292; Acute respi ratory di stress syndrome (2), p294; Heart

fai lure—assessment, p324; Heart fail ure—management, p326; Acute renal fai lure—diagnosis, p332; Acute renal

fai lure—management, p334; Diarrhoea, p340; Jaundi ce, p358; Anaemi a, p400; Platel et disorders, p406; Neutropeni a,

p408; Hyperkalaemi a, p420; Infecti on—di agnosi s, p480; Infecti on—treatment, p482

Ovid: Oxford Handbook of Critical Care

Editors: Singer, Mervyn; Webb, Andrew R.

Title: Oxford Handbook of Critical Care, 2nd Edition

Copyri ght ©1997,2005 M Si nger and A R Webb, 1997, 2005 Publ ished in the United States by Oxford Universi tyPress Inc

> Table of Co ntents > Metabo lic Dis orders

Metabolic Disorders

Electrolyte management

A balance must be achieved between el ectrol yte i ntake and output Consider:

Altered i ntakeImpaired renal excretionIncreased body l ossesBody compartment redi stributi on (e.g i ncreased capil lary l eak, secondary hyperal dosteronism)

As wel l as Na+ and K+, consi der Mg2+, Ca2+, Cl- and PO43- bal ance

Plasma el ectrol yte values are poorly reflecti ve of whole body stores; however, excessively high or l ow plasma levels

may induce symptoms and deleterious physiological and metabolic sequelae

Water bal ance must al so be taken i nto account; depleti on or excess repletion may respectively concentrate or di lute

electrol yte level s

The usual daily requi rements of Na+ and K+ are 60–80 mmol

Gravi tational peripheral oedema implies i ncreased total body Na+ and water, though intravascul ar sal t and water

depletion may coexist

P.417

See also:

Electrol ytes

, p146; Urinalysis, p166; Hypernatraemi a, p416; Hyponatraemia, p418; Hyperkal aemia, p420; Hypokalaemia, p422;

Hypomagnesaemia, p424; Hypercalcaemi a, p426; Hypocal caemia, p428; Hypophosphataemia, p430

Hypernatraemia

Clinical features

Thi rst, lethargy, coma, seizures, muscular tremor and rigi dity, and an increased risk of intracrani al haemorrhage

Thi rst usually occurs when the plasma sodium ri ses 3–4 mmol /l above normal Lack of thi rst i s associated wi th

central nervous system disease

Treatment

Depends upon the cause and whether total body sodium stores are normal , l ow or elevated and body water i s normal

or low

Rate of correction

If hyperacute (<12 h), correcti on can be rapid

Otherwise, aim for gradual correction of plasma sodium level s (over 1–3 days), particul arl y i n chronic cases (>2days' durati on), to avoid cerebral oedema through sudden l owering of osmol ali ty A rate of plasma sodium

loweri ng <0.7 mmol/h has been suggested

Hypovolaemia

If hypovol aemia is accompani ed by haemodynamic alterations, use coll oi d i nitial ly to restore the ci rculation

Otherwise, use isotonic sal ine

Artifi ci al col loi d sol uti ons consi st of hydroxyethyl starches (e.g Hespan, EloHAES) or gel ati ns (e.g Gel ofusin,Haemaccel) di ssolved i n i sotonic sal ine

Normal total body Na (water loss)

Water replacement either PO (addition to enteral feed) or as 5% glucose IV Up to 5l/day may be necessary

If cranial diabetes i nsi pi dus (CDI): restrict salt and give thiazide di ureti cs Compl ete CDI wi ll requi redesmopressin (10µg bd intranasall y or 1–2µg bd IV) whereas partial CDI may require desmopressin but oftenresponds to drugs that i ncrease the rate of ADH secretion or end-organ responsiveness to ADH, e.g

chl orpropami de, hydrochl orthi azi de

If nephrogeni c DI: manage by a l ow sal t diet and thiazi des High dose desmopressin may be effective Considerremoval of causative agents, e.g l ithium, demecl ocycli ne

Low total body Na (Na and water losses)

Treat hyperosmol ar non-ketotic diabetic crisi s, uraemi a as appropriate

Otherwise consi der 0.9% sal ine or hypotoni c (0.45%) sal ine Up to 5 l/day may be needed

Increased total body Na (Na gain)

Water replacement either PO (addition to enteral feed) or as 5% glucose IV Up to 5l/day may be necessary

In addi ti on, furosemi de 10–20 mg IV prn may be necessary

Causes of hypernatraemia

Low total body Na Renal losses: diuretic excess,

osmotic diuresis (glucose, urea, mannitol)

[Na+] >20 mmol/l

iso-or hypotonic

Extra-renal losses: excess

+] <10 mmol/l hypertonic

Normal total body Na Renal losses: diabetes insipidus [Na+] variable hypo-,

iso- or hypertonic

Extra-renal losses: respiratory

+] variable hypertonic

Increased total body Na Conn's syndrome, Cushing's

syndrome, excess NaCl, hypertonic NaHCO3

[Na+] >20 mmol/l

iso-or hypertonic

See also:

Haemo(dia)fil trati on (1), p62; Haemo(dia)fi ltration (2), p64; Enteral nutri tion, p80; Parenteral nutrition, p82;

Electrol ytes

, p146; Urinalysis, p166; Crystal loi ds, p176; Col loi ds, p180; Di uretics, p212; Electrolyte management, p414; Di abeti c

ketoacidosis, p442; Hyperosmolar diabetic emergenci es, p444

Hyponatraemia

Clinical features

Nausea, vomi ting, headache, fatigue, weakness, muscular twitchi ng, obtundation, psychosis, seizures and coma

Symptoms depend on the rate as wel l as the magnitude of fal l in the pl asma [Na+]

Treatment

Rate and degree of correction

In chroni c hyponatraemia correcti on should not exceed 0.5 mmol/l /h in the fi rst 24 h and 0.3 mmol /l/hthereafter

In acute hyponatraemia the i deal rate of correcti on is controversi al though el evations in plasma Na+ can befaster, but <20 mmol/l /day

A plasma Na+ of 125–130 mmol /l is a reasonable target for i ni tial correction of both acute and chronic states

Attempts to achieve normo- or hypernatraemi a rapi dly shoul d be avoi ded

Neurol ogi cal compl icati ons, e.g central pontine myel inolysis, are related to the degree of correction and (inchroni c hyponatraemia) the rate Premenopausal women are more prone to these compli cations

Extracellular fluid (ECF) volume excess

If symptomati c (e.g seizures, agi tation), and not oedematous, 100 ml ali quots of hypertonic (1.8%) sali ne can

be given, checki ng plasma level s every 2–3 h

If symptomati c and oedematous, consider furosemide (10–20 mg IV bolus prn), mannitol (0.5g/kg IV over 15–20min), and replacement of uri nary sodi um losses wi th ali quots of hypertoni c sal ine Check pl asma l evels every2–3 h Haemofiltration or di al ysi s may be necessary if renal fai lure is establ ished

If not symptomatic, restrict water to 1–1.5 l /day If hyponatraemia persi sts, consider inappropriate ADH (SIADH)secretion

If SIADH likely, give isotoni c sali ne and consi der demeclocycl ine

If SIADH unl ikely, consi der furosemi de (10–20 mg IV bolus prn), manni tol (0.5 g/kg IV over 15–20 min), andreplacement of uri nary sodi um l osses wi th ali quots of hypertoni c sali ne

Check plasma levels regul arl y Haemofiltration or dial ysi s may be necessary if renal fai lure is establ ished

Extracellular fluid volume (ECF) depletion

P.420

If symptomati c (e.g seizures, agi tation), gi ve i sotoni c (0.9%) sal ine Consider hypertonic (1.8%) sali ne

If not symptomatic, gi ve isotonic (0.9%) saline

Many patients achieve normonatraemia by spontaneous water diuresi s

Use isotonic solutions for reconsti tuting drugs, parenteral nutriti on, etc

Hyponatraemia may i ntensi fy the cardi ac effects of hyperkal aemia

A true hyponatraemi a may occur with a normal osmolal ity in the presence of abnormal solutes e.g ethanol ,ethylene glycol , gl ucose

Causes of hyponatraemia

[Na+]

ECF volume depletion Renal losses: diuretic excess, osmotic diuresis (glucose,

urea, mannitol), renal tubular acidosis, salt-losing nephritis, mineralocorticoid deficiency

>20 mmol/l

Extra-renal losses:

vomiting, diarrhoea, burns, pancreatitis

<10 mmol/l

Modest ECF volume excess (no oedema) water intoxication (NB post-operative, TURP syndrome), inappropriate ADH secretion, hypothyroidism, drugs (e.g.

carbamazepine, chlorpropamide), glucocorticoid deficiency, pain, emotion.

>20 mmol/l

acute and chronic renal

ECF volume excess (oedema) nephrotic syndrome, cirrhosis, heart failure <10 mmol/l

Causes of inappropriate ADH secretion

Neoplasm, e.g l ung, pancreas, lymphomaMost pulmonary l esi ons

Most central nervous system lesionsSurgical and emoti onal stress

Glucocorticoid and thyroid deficiencyIdi opathi c

Drugs, e.g chl orpropami de, carbamazepi ne, narcotics

See also:

Haemo(dia)fil trati on (1), p62; Haemo(dia)fi ltration (2), p64; Enteral nutri tion, p80; Parenteral nutrition, p82;

Electrol ytes

, p146; Urinalysis, p166; Crystal loi ds, p176; Col loi ds, p180; Di uretics, p212; Acute renal fail ure—di agnosis, p332;

Acute renal fai lure—management, p334; El ectrolyte management, p414; Di abetic ketoacidosi s, p442; Hyperosmol ar

diabetic emergenci es, p444

Hyperkalaemia

Plasma potassium depends on the balance between i ntake, excretion and the di stributi on of potassi um across cell

membranes Excreti on is normal ly controll ed by the ki dneys

Potassi um poi soning

Clinical features

Hyperkalaemi a may cause dangerous arrhythmi as including cardiac arrest Arrhythmias are more cl osely related to

the rate of rise of potassi um than the absolute level Cl ini cal features such as paraesthesiae and areflexic weakness

are not clearl y related to the degree of hyperkal aemia but usual ly occur after ECG changes (tall ‘T’ waves, flat ‘P’

waves, prolonged PR interval and wide QRS)

Management

Potassium restricti on i s needed for al l cases and haemodi afi ltration or haemodialysis may be needed for resi stant

cases

Cardiac arrest associated with hyperkalaemia

Sodium bi carbonate (8.4%) 50–100 ml should be gi ven in addition to standard CPR and other treatment detail ed

bel ow

Potassium >7 mmol/l

Cal cium chl ori de (10%) 10 ml should be given urgently in additi on to treatment detai led below Although calcium

chl oride does not reduce the plasma potassium, i t stabil ises the myocardium agai nst arrhythmias

Clinical features of hyperkalaemia or potassium >6 mmol/l with ECG changes

Gl ucose (50 ml 50%) and solubl e i nsulin (10 i u) should be gi ven IV over 20 min Blood gl ucose shoul d be monitored

every 15 min and more glucose given i f necessary In addition, cal cium resonium 15 g qds PO or 30 g bd PR can be

consi dered

See also:

Haemo(dia)fil trati on (1), p62; Haemo(dia)fi ltration (2), p64; Enteral nutri tion, p80; Parenteral nutrition, p82;

Electrol ytes

, p146; Urinalysis, p166; Crystal loi ds, p176; Diuretics, p212; Cardi ac arrest, p272; Bradyarrhythmias, p318; Acute

renal fai lure—diagnosis, p332; Acute renal fail ure—management, p334; Electrolyte management, p414;

Rhabdomyol ysis, p528

Hypokalaemia

Plasma potassium depends on the balance between i ntake, excretion and the di stributi on of potassi um across cell

membranes Excreti on is normal ly controll ed by the ki dneys

Causes

Inadequate intakeGastrointestinal losses (e.g vomiti ng, di arrhoea, fi stula losses)Renal l osses (e.g diabetic ketoacidosis, Conn's syndrome, secondary hyperal dosteroni sm, Cushi ng's syndrome,renal tubular acidosi s, metaboli c al kal osis, hypomagnesaemia, drugs i ncluding di ureti cs, steroids, theophyll ines)Haemofi ltration losses

Potassi um transfer into cel ls (e.g acute alkalosis, glucose infusion, i nsuli n treatment, famil ial peri odi cparalysis)

Clinical features

Arrhythmi as (SVT, VT and Torsades de Pointes)ECG changes (ST depression, ‘T’ wave flattening, ‘U’ waves)Metabol ic al kal osi s

Consti pationIleus

Weakness

Wherever possible, the cause of potassium l oss shoul d be treated.

Potassi um replacement shoul d be i ntravenous wi th ECG monitori ng when there i s a cl inically si gnifi cantarrhythmi a (20 mmol over 30 min, repeated accordi ng to levels)

Slower intravenous replacement (20 mmol over 1 h) shoul d be used where there are cl ini cal features wi thoutarrhythmi as

Oral supplementati on (to a total i ntake of 80–120 mmol/day, incl udi ng nutritional input) can be given wherethere are no cli ni cal features

See also:

Enteral nutrition, p80; Parenteral nutriti on, p82; Electrolytes

, p146; Urinalysis, p166; Crystal loi ds, p176; Diuretics, p212; Steroids, p262; Cardiac arrest, p272;

Tachyarrhythmi as, p316; Electrolyte management, p414; Metabol ic alkalosis, p436; Di abeti c ketoaci dosis, p442;

Post-operati ve intensive care, p534

Magnesium is primari ly an intracell ul ar ion invol ved in the production and util isati on of energy stores and i n the

mediation of nerve transmissi on Low pl asma l evels, which do not necessaril y refl ect ei ther intracell ul ar or whole

body stores, may thus be associated with features related to these functi ons:

Confusi on, irri tabil itySei zures

Muscle weakness, lethargyArrhythmi as

Symptoms rel ated to hypocalcaemia and hypokalaemia which are resi stant to calci um and potassiumsupplementation respecti vel y

Normal pl asma l evels range from 0.7–1.0 mmol/l ; severe symptoms do not usual ly occur until levels drop bel ow 0.5

mmol/l

Management

Where possible, identify and treat the cause

For severe, symptomati c hypomagnesaemi a, 10 mmol of magnesium sulphate can be given IV over 3–5 min Thiscan be repeated once or twice as necessary

In l ess acute situati ons or for asymptomatic hypomagnesaemia, 10–20 mmol MgSO4 soluti on can be given over1–2 h and repeated as necessary, or accordi ng to repeat pl asma l evel s

A continuous IV infusion (e.g 3–5 mmol MgSO4 sol uti on/h) can be given; however, thi s i s usuall y reserved fortherapeutic indicati ons where supranormal pl asma l evel s (1.5–2 mmol/l ) of magnesium are sought, e.g

treatment of supraventri cul ar and ventricular arrhythmias, pre-eclampsi a and ecl ampsia, bronchospasm

Oral magnesi um sul phate has a l axati ve effect and may cause severe diarrhoea

High plasma l evels of magnesium may devel op in renal fai lure; cauti on should be appli ed when administering IVmagnesi um

See also:

Enteral nutrition, p80; Parenteral nutriti on, p82; Calcium, magnesi um and phosphate, p148; Diuretics, p212;

Asthma—general management, p296; Tachyarrhythmias, p316; Electrolyte management, p414; Generali sed seizures,

p372; Pre-eclampsi a and ecl ampsia, p538

Immobil isati onRarely, thyrotoxicosi s, Addison's di sease

Clinical features

Usuall y become apparent when total (i oni sed and un-i oni sed) plasma levels >3.5 mmol /l (normal range 2.2–2.6

mmol/l ) Symptoms depend on the patient's age, the duration and rate of i ncrease of pl asma calcium, and the

presence of concurrent medi cal condi ti ons

Nausea, vomiting, weight loss, pruri tusMuscle weakness, fatigue, lethargyDepression, mania, psychosi sDrowsi ness, coma

Abdomi nal pain, constipationAcute pancreati tis

Peptic ul cerati onPolyuria, renal calculi , renal fail ureArrhythmi as

Cal cium, magnesium and phosphate, p148; Diuretics, p212; Steroids, p262; Acute renal fail ure—diagnosis, p332;

Acute renal fai lure—management, p334; Pancreatitis, p354; Electrol yte management, p414; Diabeti c ketoaci dosis,

p442; Thyroi d emergencies, p446; Hypoadrenal cri sis, p448

Hypocalcaemia

Causes

Associ ated with hyperphosphataemi a:

Renal fail ureRhabdomyolysisHypoparathyroidi sm (includi ng surgery), pseudohypoparathyroidismAssoci ated with low/normal phosphate:

Critical i ll ness i ncluding sepsi s, burnsHypomagnesaemi a

PancreatitisOsteomalaciaOver-hydrationMassive bl ood transfusion (citrate-binding)Hyperventi lation and the resul ting respiratory alkalosis may reducethe ionised plasma cal cium fracti on andinduce cl ini cal features of hypocalcaemia

Clinical features

These usuall y appear when total plasma cal cium l evels <2 mmol /l and the i oni sed fraction i s <0.8 mmol/l

Tetany (includi ng carpopedal spasm)Muscul ar weakness

Hypotensi onPeri oral and peripheral parasthesiaeChvostek & Trousseau's si gns

Prol onged QT intervalSei zures

If hypotensive or cardiac output i s decreased fol lowing admi nistrati on of a calci um antagonist, give 5–10 ml 10%

cal cium chlori de sol uti on over 2–5 min

5