Electrolyte Disturbance

in cancer patients
Resident.Dr /Doaa Abdelwahab
 Potassium level disturbance
normal level of serum potassium 3.5-5.5 mEq/L
Hypokalemia (potassium level less than 3.5 mEq/L)
the most common electrolyte abnormality in cancer
patients.
causes of hypokalemia in cancer patients
1-decreased potassium intake : nausea,anorexia
2-increased potassium loss : vomiting , Diahrrea ,Type 1 renal hyperkalemia in cancer patient
tubular acidosis
3-Drug induced >
loop Diuretics, aminoglycosides
beta adrenergic agonist
platinum based chemotherapy (cisplatin, carboplatin,
alkylating agents (holoxan, endoxan)
steriods (pharmacologic administration, cushing syndrome
as paraneoplastic syndrome )
4-others :
alkalosis (as in vomiting),
Magesium depletion ( Magnesium is directly involved in the
regulation of calcium and potassium metabolism).
Hyperkalemia(potassium level more than 5.5 mEq/L)
a common electrolyte disorder in cancer patients.
causes :
1- Inappropriate high potassium content in intravenous fluid
and total parenteral nutrition are common causes of
2- decreased excretion: acute or chronic renal failure
3-Drug induced
potassium-sparing diuretics(spironolactone)
Beta blockers (release of intracellular potassium), ACEIs
digoxin.(decrease K excretion )
NSAIDS
4-significant extracellular shift potassium:
tumorlysis syndrome.
metabolic acidosis( eg:DKA)
massive blood transfusion
• Clinical manifestations:
• mild hypokalemia (3-3.5 mEq/L )>
usually asymptomatic
• Symptomatic sever hypokalemia(less
than 3 mEq/L) :
arrhythmia,ms weakness ,paresthesia ,
even paralysis
• ECG changes :prolonged PR interval ,
depressed ST segment , flattened T
wave, prominent U wave
• clinical manifestations :
• up to 7.5 mEq/L > usually
asymptomatic espically in patients
with CKD
• . At greater than 7.5 mEq/L,
nonspecific symptoms such as muscle
weakness, cramping, and paralysis of
different muscle groups may occur.
• ECG changes:
• VF/VT, absent P wave, wide QRS
• ST segment depression,
bradycardia,first degree heart block
• managment :
1-high potassium diet : bananas,oranges, potatoes,tomatoes,
carrots, dried fruits (dates),Kiwis, Avogado
2-potassium repalcment according to K level
-mild-moderate hypokalemia (2.6-3.5 mmol/l) >oral
potassium(eg:sando-K)
Mild >2 tablets OD/BD Moderate> 2tab BD/TD
-sever hypokalemia (< 2.5 mmol /L) : IV potassium (slow -
infusion) eg: 40 mmol potassium(2 amp 10 ml of 15%KCL) in 1000
ml of 0.9%NaCL over at least 4 hours every 12 hr
through periphral or central line
(NB: rapid infusion an lead to hyperkalemia , heart block, even
cardiac arrest , phlebitis, pain at the injection site)
NB: in life threatning conditions in ICU that need administration
of higher concentrated potassium solution over less duration we
use central line (40mmol of potassium in 100ml of 0.9% sodium
chloride over at least 2–4hours via a central line in an HDU/ITU
setting.)
• - serum potassium level monitoring until within normal range
• -ECG monitoring
• check Magnesium level and replace if low (as 40-50% of
patients with hypokalemia also have hypomagnesemia)
3--treatment of the underlyning cause if possible
• managment :
1-Low potassium diet and stop any medications that
may contribute to hyperkalemia if possible
*treatment of hyperkalemia according to severity of
hyperkalaemia:
▪ Mild-moderate (up to 6.4mmol/L) :
-give fluids to enhance urinary potassium excretion
• If potassium >6.5mmol/L or ECG changes>>
10 units of short-acting insulin (e.g.Actrapid®) and
250ml of 10% glucose over 30–60minutes (with
monitoring Glucose level )
10ml of 10% calcium gluconate IV over two minutes
2.5–10mg nebulised salbutamol( with caution in
patients with ischaemic heart disease)
IV sodium bicarbonate if patient is acidotic (pH 7.1–
7.3), for example due to DKA
*check potassium level at least twice daily until
<6mmol/L.loop
in refractory cases >diuretics and Emergent
hemodialysis may be used
3-treatment of the underlyning cause
 case senario of hypokalemia
• male ptn , 29 yo , case of advanced rectal ca with bladder infiltration ,ptn
started neoadj xelox > ended CCRT 4/2022
*presented by
progressive vomiting,
scr: 3.8
k:2.5
(ptn has CKD , Rt PCN )
---------------------
• causes of hypokalemia : vomiting (K loss , alkalosis )
• on hydration > scr decreased to 2.5
• on IV potassium 2 amp in 1 lit 0.9% saline over 4 hr > K elevated to 3.7 >4
 Calcium level disturbance
The normal range of total calcium is usually (8–10mg/dl )
Hypocalcemia:(total calcium <8 mg/dl) Hypercalcemia (total calcium >10 mg/dl)
In hospitalized cancer patients, hypocalcemia is about observed in 10–15 % of cancer patients.(poor
13.4 % prognosis,with short survival durations. )
causes : Causes:
1- pseudohypoalcemia 1-The most common cause is paraneoplastic syndrome :
hypoalbuminemia leads decrease in total calcium level, PTH-related peptide secretion ,interleukin-1 and -6,
but ionised calcium levels remain relatively prostaglandins, and tumor necrosis factor, can mediate
stable> pseudohypoalcemia ) hypercalcemia in cancer patients.
2- Increased levels of 1,25-dihydroxy vitamin D 3 in
○ Vitamin D malabsorption/deficiency, low exposure to patients lymphoma.
UV light(bed ridden cancer patients)
3-Extensive lytic bone metastasis(eg: multiple myeloma
or breast cancer)
•Hypoparathyroidism : Thyroid or parathyroid surgery, 4- hyperparathyroidism
Radical neck surgery

• Drugs: Bisphosphonates, Cisplatin,Calcium channel Drugs :thiazide diuretics

blocker overdose

-assosiated with Hypomagnesaemia

• Symptoms/signs
• Chvostek’s sign (tapping over the
facial nerve causes facial twitching),
• Trousseau’s sign (carpopedal spasm
when brachial artery occluded),
• tetany, depression, perioral
paraesthesiae, confusion
• ECG changes: prolonged PR interval,
prolongedQT interval,ST segment
depression , T wave inversion, heart
block
• CNS symptoms :lethargy, coma,
• GIT symptoms are constipation,
and pancreatitis
• Renal :polyuria,nephrolithiasis,
and nephrocalcinosis.
• Musculoskeletal symptoms are
myalgia, arthralgia, and
weakness.
• CVS: sinus arrest, and AV block.
• managment: • Management :
1-high calcium diet (dairy products,soybeans,salmon) and Correct
abnormalities in potassium and magnesium 1- : minimise dairy products and stop
2-calcium replacement : medications that contribute to hypercalcemia
Serum ca++ should be corrected in ptn with
hypoalbuminemia(common cause)
if possible (e.g., calcium-containing
(corrected calcium level = [0.8 × (normal average albumin level(4)− medications, thiazide diuretics)
patient’s albumin level)] + sr.calcium)
2-increase calcium excretion
*Mild – moderate (calcium 1.88–2.11mmol): oral calcium
replacement: 1 tablet BD of Calcichew® or Adcal® (plus vitamin D if The initial and first-line treatment is hydration
vitaminD deficient).
Given after meals to maximise absorption.
and loop diuretic(if patient not hypovolemic)
*Moderate to severe (calcium <1.88mmol/L): -Bisphosphonates . Zoledronate (4–6 mg
10ml of 10% calcium gluconate(Amp)IV , diluted in 100 ml D5W intravenously over 30 min)
over 10-20 minute, can be repeated as required
3- Second-line agent: calcitonin (salmon
• ○ ECG monitoring (particularly in cardiac patients or on digoxin as calcitonin 4 IU/kg S.C every 12 h)
it can potentiate digoxin toxicity.).
• Serum calcium monitoring until within the normal range. -monitor calcium level until within normal
3-in patients who are resistant to therapy,Consider checking the
underlyning causes
4-treatment of the cause if possible :Primary
-PTH levels hyperparathyroidism can be cured via
-Serum 25-hydroxyvitamin D levels in confirming vitamin D parathyroidectomy .
deficiency
 case senario of hypocalcemia
• female ptn , 32 yo , case of cancer cervix >CCRT >developed Rt inguinal and bone mets
>recieved pall Rth Rt inguinal LN
• run on taxol-carboplatine then Gem single agent
• back pr on Rt kidney with ealy CKD .

• 6/2022 presented on wheelchair , bilat LL edema , total ca 7.6

• causes of hypocalcemia :
-pseudohypoalcemia d.2 hypoalbuminemia
-Vitamin D deficiency, low exposure to UV light(bed ridden)

• K 2.7> oral K+ 2tablets BD

• Na 127 ,s cr 2.2 > IV hydration with 0.9% NaCL
• total ca 7.62 > oral ca+vit D one tab daily after meal
 Magnesium level disturbance
(normal plasma level of magnesium= 1.5-3 mg/dl )
hypomagnesemia (plasma magnesium less than 1.5 mg/dL ) Hypermagnesemia(plasma magnesium more than 3 mg/dL )
Seen in 17% of hospitalized cancer patients Uncommon
usually assosiated with hypokalemia and hypocalcemia
Causes : Major causes :
1-Gastrointestinal: diarrhoea, vomiting, surgical resection, 1-renal failure
malabsorption, starvation
2- endocrinal and renal causes :
uncontrolled diabetes, ketoacidosis, hyperthyroidism
tubular defects, polyuria.

• Drugs: 2-or excessive Magnesium containing medications intake in

○ Anti-cancer therapies: cisplatin, carboplatin (less than presence of renal insuffiency eg :
cisplatin), -Magnesium containing antacids or laxative
○ Diuretics. -magnesium enema
○ Aminoglycoside antibiotics.
○ Amphotericin B.
○ Bisphosphonates.
○ Proton pump inhibitors.
clinical manifestations as in • clinical manifestations :
hypocalcemia -Main presentation :diahrrea
• Chronic hypomagnesaemia can occur -hypotension,
after three weeks of chemotherapy
(e.g. with cisplatin) and persist for - bradycardia and arrhythmias.
months
• • Associated with hypocalcaemia and
hypokalaemia.
Management :
1- Correct calcium and potassium abnormalities.
2- high magnesium diet : green leafy vegetables, seeds, nuts, peas,
beans .
3-Magnesium replacement when the serum magnesium level is
repeatedly below normal and symptomatic
• Mild – moderate hypomagnesmia (still above 0.7 mg/dl): oral
magnesium glycerophosphate 1–2 tablets TDS , diarrhea may be a
dose-limiting side effect
• Severe (<0.7 mg/dl ): IV (5g )magnesium sulphate in 1L of 0.9%
sodium chloride or 5% glucose over 3–5hours, with monitoring
-Mg level (risk of hypermagnesaemia in Patients with renal failure )>
DR by 50–75% in pt with renal faliur)
-cardiac monitoring ( risk of cardiac arrest.if Rapid administration)
-BP (risk of hypotention)
• Emergencies:
• ○ Arrythsmia (Torsade de points): (2g) of 50% magnesium sulphate
IV over 15 minutes with cardiac monitoring
• ○ Seizure: (2g) magnesium sulphate IV over 10 minutes with
cardiac monitoring
• ○Recheck magnesium after 48 hours(Magnesium takes 36–
48hours to distribute to body tissues )
• Management :
1-Discontinuation of Magnesium containing medications
is the first step.
2-need treatment only if:
*symptomatic severe hypermagnesemia
( hypotension ,arrhythmia, respiratory depression ):
10ml of 10% calcium chloride IV removes magnesium
from serum
* life- threatening hypermagnesemia(8 mg/dL):
Emergent dialysis
• NB: Saline diuresis(saline +fursomide) not recommended
-need normal renal function and adequate cardiovascular function
- However,will lead to ca excretion > hypocalcaemia > worsening
symptoms and signs of hypermagnesmia
(arrhythmia,hypotention)
 Case senario of
hypocalcemia,hypokalemia,hypomagnsemia
• female ptn , 41 yo , case of MBC to bone , liver, lung
• on xeloda-tykerb
• on zometa

• presented 6/2022 by repeated vomiting and diarrhea

• Ca (ionized) : 1.18 mmol/l
• K: 2.29 mmol/l
• Mg:2.1 mg/dl
• ------------------------------
• recieved antiemitics and PPI , IV Ca Gluconate ,IV potassium
• ca (Ionized) : 2 mmol/l
• K: 3.17 mmol/l
• Mg:1.67 mg/dl ( lab reference 1.7-2.5)
 Sodium level disturbance
(The normal range for sodium is usually 135–145mmol/L. )
Hyponatraemia(sodium level less than 135 mEq/L)
a common problem in oncology patients
causes :
1- Overhydration with IV fluids low in electrolyts (5% dextros)
2-hypervolemic hyponatremia :
-Cirrhosis, nephrotic syndrome, Congestive HF
-SIADH( 11–15% of patients with SCLC )
3-Hypovolemic hyponatremia :-
Git loss ( Diarrhea, vomiting), Renal salt loss
3-Drug induced :
diuretics
anti-cancer drugs: cisplatin, carboplatin, cyclophosphamide,
ifosfamide,vinblastine, vincristine, methotrexate, interferon
○ Opioids, NSAIDs ○ PPIs: omeprazole
○ Antidepressants: SSRIs, tricyclics,
○ Anti-epileptics: sodium valproate, carbamazepine
○ Antipsychotics: haloperidol, risperidone
Hypernatremia (sodium level greater than 145 mEq/L)
causes :
1-excess sodium intake: . excessive IV 0.9% sodium chloride,
total parenteral nutrition, .
2-dehydrated patients :
increased water loss include : vomiting ,diarrhea.
inadequate water intake can have many causes, including
-GI tract obstruction
-chemotherapy- or radiotherapy-induced mucositis.
-dysfunction of the thirst center in hypothalamus owing to a
primary brain tumor or brain metastasis
-Diabetes insipidus
3- Drugs that decrease the effect of antidiuretic hormone
include vinblastine, amphotericin
• Symptoms/signs: • Symptoms/signs:
• become symptomatic when the 1-signs of dehydration
sodium concentration is <120mmol/L: thirst
confusion, irritability, headache, dry tounge
hypertension, oedema, postural hypotension
muscle weakness, cardiac failure and seizures. oliguria)

2- CNS changes
if the sodium level is greater than 160
mEq/L:
confusion, irritability,coma and seizures.
• Management :
1-Asymptomatic patients with chronic
hyponatraemia (and not hypovolemic ,edemtous) :
*Restricted free water intake : to 500 – 800 mL of
free water per day
*Increased free water excretion:-
-loop diuretics such as furosemide
-if fluid restriction is ineffective(In patients with
SIADH) consider demeclocycline 600–1200mg daily
2-Symptomatic patients :
slow correction with 0.9% sodium chloride(0.5–1L
over 2–4hours )
• severely symptomatic patients :hypertonic saline(3
%NaCl) at a rate of 1 mL/kg/h.
• Decreased sodium loss : Fludrocortisone: 0.1–0.6
mg a day orally.
3-• Treatment of the underlying etiology of
hyponatremia
• managment :
1- Mild or moderate hypernatraemia:
- water orally if possible in prescribed amount per
day in regular basis
- A low-salt diet
- solutions low in electrolytes (e.g dextrose 5 % ).
slowly IV (e.g. approximately 4L in 24 hours).
- 0.9% NaCL (can be used especially if
hypovolaemic) as this results in less marked fluid
shifts.
2-Severe hypernatraemia (> 170mmol/L) in
hypovolaemic patients:
• 0.9% sodium chloride should be used initially to
avoid rapid drops in serum sodium concentration,
which could lead to cerebral oedema.
3-Treat the underlying cause if possible.
 case senario of hyponatremia
• male ptn ,54 yo , case of rectal carcinoma recieved neoadj CCRT ,
• underwent surgery then adj chemo ended 6/2020 ,
• 7/2022 isolated pelvic recurrence and presented by
• repeated vomiting and dehydration, ptn already on PPI ,and morphin

• Na =124 (asymptomatic)
• s cr 2.4

• cause of hyponatremia :
• vomiting (Na loss )
• chronic use of PPI
• opioid use

• ttt:
• hydration with with 0.9% sodium chloride > scr =1.1, Na elevated
 phosphate level disturbance
normal serum phosphate level (2.8-4.5 mg/dl)
significant Hypophosphatemia (serum phosphate < 2 mg/dl) hyperphosphatemia (serum phosphate >4.5 mg/dl)
found in 30% of cancer patients Rare (found in 2.5% of cancer patients)

causes : Causes:
chronic hypophosphatemia: 1• Tumour lysis syndrome
-extensive osteoblastic metastasis of prostate, breast, lung 2• Acute or chronic kidney disease
(Chronic hypophosphatemia together with hypocalcemia) 3-Hypoparathyroidism
-progressing leukemia or lymphoma (e.g., Burkitt lymphoma)
-any hepatic affection (significant role in phosphate
hemostasis):HCC , Rt hepatic lobectomy
-hyperparathyroidism (accelerated bone formation),
-renal tubular defect (defective phosphate reabsorbtion)

Acute hypophosphatemia :intracellular shift of phosphate

through :
Respiratory alkalosis,
gram-negative sepsis 4-• metabolic acidosis

Drug induced :
granulocyte colony-stimulating factors(GCSF)
chemotherapeutic drugs :platinum compounds and alkylating 5-• Drugs: phosphate-containing laxatives in patient with renal
agents (e.g., ifosfamide). impairment
• clinical manifestations : • clinical manifestations :
• chronic hypophosphatemia: • Asymptomatic
- Muscle weakness and bone aches is Most symptoms are non-specific and are
the most common complaint due to the underlying cause or associated
-Osteomalacia, waddling gait, hypocalcaemia(fatigue, anorexia, nausea,
pseudofractures, and fractures tetany, perioral numbness/tingling.)
• muscle weakness, bone or joint pain.
• Acute hypophosphatemia :neurologic
findings :cofusion , disorientation
-muscle paralysis, seizure, and coma,
are observed only when the serum
phosphate level is less than 0.8 mg/dL.
• managment :
• Patients with hypocalcaemia should have this
corrected prior to phosphate administration to
prevent further hypocalcaemia
• Asymptomatic patients with mild-moderate
hypophosphatemia(still above 0.3 mmol /dl)
• ○ Give oral phosphate, for example two tablets
BD/TDS of Phosphate-Sandoz®
• Severe hypophosphataemia or symptomatic
patients ,or
• ptn on Oral magnesium, calcium or aluminium
containing products can bind to oral Phosphate-
Sandoz® and prevent its absorbtion :
• administer IV phosphate 0.2–0.5mmol/kg/day ,up
to a maximum of 50mmol
• Treatment of the underlying cause if possible
There is no CTCAE grading for hyperphosphataemia
Management according to severity of symptoms
• Acute hyperphosphateamia:
*resolves within 6–12hours In patients with normal
renal function
*Can be associated with symptomatic hypocalcaemia
and be life-threatening:
- IV fluids (0.9% sodium chloride) can increase
phosphate excretion
-Dextrose and insuline (intracellular shift of phosphate)
-haemodialysis, particularly if impaired renal function.
• Chronic hyperphosphataemia:
low phosphate diet : minimise dairy products, fish,
chocolate, bran, organ meats (e.g. liver).,dark chola
○ in patients with renal failure >consider
nonabsorbable phosphate binder that are aluminum-
and calcium-free(calcium and Al compounds percipitae
renal impairment):(800–1600 mg of sevelamer with
each meal)