Hypocalcemia Management
Approach to Hypocalcemia
(2) Diagnosis
Hypocalcemia: Total serum calcium < 8.5
mg/dL or ionized calcium
< 4.65 mg/dL
Severe Hypocalcemia:
Total serum calcium ≤
7.5 mg/dL or ionized calcium ≤ 3.6 mg/dL
(3) Management
Alarms signs or severe hypocalcemia
No alarm signs or mild hypocalcemia
IV Calcium
Initial bolus: 10 mL of 10% calcium gluconate (1g) diluted in 100 mL N/S or dextrose over 10 minutes is recommended.
Continuous infusion:
• Rate: 5 to 20 mg/kg/h
• Example: 10% calcium gluconate in 100 mL N/S
over an hour delivers 10 mg/kg/h in a 100-kg patient
Treat
Oral Calcium: 1-2 g elemental calcium daily (e.g., calcium carbonate/citrate).
Vitamin D:
- Hypoparathyroidism:
Calcitriol 0.25-0.5 mcg twice daily.
- Vitamin D Deficiency:
50,000 IU vitamin D2/D3
weekly for 6-8 weeks, then
800-1000 IU daily.
Magnesium: correct according y
Treat Hypomagnesemia
2g magnesium sulfate IV
over 2-15 mins, then 1 g/hour in 100 mL fluid until normal serum magnesium.

Hypocalcemia: Management

Hyperkalemia
Consider repeating labs
To exclude pseudo-hyperkalemia
Initial assessment
(1) ECG: Peaked T-wave, wide QRS, absent P wave, sinusoidal rhythm, bradycardia or VT
(2) Signs of weakness or paralysis
Moderate (6-6.5)
+ Normal ECG
ECG Changes
Normal
Peaked T-Wave
Wide QRS
Sinusoidal
rhythm
STEP 2: Shift
Potassium
Intracellularly
1. Insulin: 10 units IV
with 25-50 g of dextrose if glucose <250 mg/dL. Give another 50 g over 5 hours if glucose was < 126 mg/dL
2. Nebulized albuterol: 10-20 mg over 10 minutes.
STEP 3: Remove excess K* levels
1. Sodium Zirconium
Cyclosilicate 10g tds (Lokelma) for up to 72 hours
2. Furosemide (if renal function is adequate): 20-40
mg IV.
STEP 4: Monitor K* and glucose
K*: at 1, 2, 4 and 6
hours then after 1 day
Glucose: every 30-60 mins for the first
6 hours then after 1 day
Consider cause and prevent recurrence
Consider stopping
ACEi, ARBs, NSAIDs and other medications
NL
Increasing severity
Severe (6.5+) OR
Abnormal ECG OR unwell patient
¡STEP 1: Stabilize the heart
- 10ml 10% Calcium Chloride over 5 min
OR
- Calcium gluconate
10%: 30 mL IV over
10 mins
Go to STEP 2, 3
and 4
Consider dialysis
(1) After consultation with a nephrologist or ICU specialist when it's refractory
(2) In hemodialysis patients if K+ > 6.5

Hyperkalemia: management

Thrombocytopenia
History and Examination
• Ask for previous platelet counts, family history, medication history (heparin) and infection exposure.
• Examine the skin for petechiae, purpura, ecchymoses, examine the liver, spleen and lymph nodes.
Repeat CBC
Are there any red flags?
Red Flags
• Major bleeding
• Platelets < 10,000
• Evidence of anemia or hemolysis
• Renal or neurologic dysfunction
• Recent exposure to heparin
• Vascular findings
• Pregnancy
• Sepsis
Peripheral Blood Smear Findings
• Clumping → Pseudo thrombocyto
-penia (EDTA)
• Schistocytes > DIC, TTP, HUS
• Teardrop, nucleated RBCs → infiltration
• Immature or dysplastic WBCs > leukemia or myelodysplasia
• Megaloblastic → B12 deficiency
• Giant platelets > inherited thrombocytpenias
Obtain history and examination
Is peripheral blood smear suggestive?
Are lab findings suggestive?
Lab Findings
• Autoimmune: ANA, APL -AB
• Infection: HIV, HCV, EBV
Consider these causes
More common
Less common
Immune
ITP
Heparin-Induced
Drug-induced
CT disorders
Acquired
HIV, Hepc, EBV
Sepsis
Hyperspleenism
B12 deficiency
Thrombotic
Microangiopathy
TTP
HUS
APS
Hematological disorders
Leukemia
Lymphoma
Myelodysplasia

Thrombocytopenia: differential diagnosis

Hyponatremia: management

Management of Hypokalemia
Approach to Hypokalemia
(1) Definition
• K+ < 3.5 mEq / L
• Mostly due to GI, urinary losses or diuretic therapy.
•
(2) Clinical features
Mild (3.0-3.5): No symptoms usually
Moderate (2.5-3.0): weakness, constipation and arrhythmias
Severe (< 2.5): muscle weakness (lower to upper body), arrhythmias then paralysis (incl. respiratory)
(3) Diagnosis
• Measure K+ levels
• Take ECG if < 3.0 or symptomatic
• ECG findings: T-inversion, ST depression, prominent u wave
• Pseudo-hypokalemia: if there is upstream of IV fluids and other electrolytes are low. No need for further evaluation if symptomatic
• Urinary K+ to identify the source of potassium loss
(5) Management
• Treat the cause if possible and not severe
• 1 mEq / L deficit: 200-400 mEq replacement needed
• If the cause was due to potassium redistribution even low rates of K+ administration can result in hyperkalemia
(6) Monitor K+ Levels
• Mild: monitor three times per week
• Moderate: monitor daily
• Severe: after each 40mEq. Continious ECG monitoring
ECG Changes
Normal
T wave inversion
ST depression
U wave
Consider the cause
(1) Decreased potassium intake: starvation, anorexia, alcoholism
(2) Gastrointestinal losses: diarrhoea, vomiting, intestinal fistulae
(3) Increased renal potassium
loss:
- Drugs: Thiazide diuretics
- Loop diuretics
(4) Transcellular K+ shift:
- Beta-agonists
- Insulin
- Metabolic alkalosis
Mild (3-3.5 mEq/L)
• Treat orally
• Dose: 40-100 mEq per day
• E.g. 2 x 10 mEq tablets three times per day
Deficit: ~ 200 mEq
Moderate (2.5 - 3 mEq/L)
• Treat orally if they can tolerate it
• Dose: 80-100 mEq per day
• E.g. 3 × 10 mEq tablets three times per day
• Alternatively via IV.
Common formulation: 40 mEg in 1,000 mL 0.9% NS
every 6 hours
• Max IV rate (peripheral IV
line): 10 mEq / hr
• Place on a continuous cardiac monitor if infusing at 10 mEg / hr
MADE WITH MEDGRAM.NET
Severe (< 2.5 mEq/L)
• Treat intravenously
• 40 mEq in 1,000 mL 0.9%
NS every 4-6 hours
preferably into a large vein
• Increase infusion rate if life-threatening to up to 20 mEq / L on a peripheral line
• Otherwise in a peripheral line, the max rate is 10 mEq / hr
• On a central line, the max rate is 40 mEq / hr

Hypokalemia: diagnosis and management

Anemia Differential Diagnosis*
MCV
Normocytic
(MCV 80 - 100 fL)
(RBCs lost, or less RBCs produced)
† WBCs
or Normalwaes
† WBCs
* Low retics
or inappropriately
† High retics
See blood smear.
‡ Low retics or normal
† High retics
(marrow is fine)
†marrow Is tine
Early Fe deficiency
‡ EPO (renal failure)
Malignancy (e.g. MM)
Marrow aplasia, suppression or
infitrration
(pancytopenia).
Spleenomegaly or
Hyperspleenism (primary or secondary
Pregnancy (RBC dilution)
B12/Fol deficiency
RBCs: Normal
RBCs: Spherocytes
or SenIStocVteS
RBCs: Sickle cells,
target cells, howell-jolly bodies
Acute Bleeding
Hemolysis
Autommune or hereditary spherocytosis
Hemoglobinopathy
(HbS, HbE, HbC)
(HbE can be microcytic)
Microangiopathic
homovic anemia:
DOC, TTP, HUS
* This graphic is provided as it is, I bear no responsibility for any errors made. All rights belong to Yan Yu (yanyu.ca). Please do not distribute without permission.
Designed by Khudhur M.
• Target cells
• Normal WBCs
Liver Disease (More lipids in RBC
memorane)
khudhur_moh
me@khudhur.com
Macrocytic
(MCV > 100fL
(V DNA synthesis, 4 Cell division)
Rule out Reticulocytosis
Abnormal blood smear
• Oval macrocytes.
• Hyper-segmented
neutroonis.
• + Retics.
• Pancvtopenia.
• Megaloblastic
anemia in marrow
• RBCs in Rouleaux formation (false increase in MCV
que to
agglutination.
Multiple Myeloma
‡ RBC
• + Folate
・ ↑ Homocysteine
(alcoholic?)
Folate deficiency
(malabsorption, increased need)
Normal Blood Smear
Drugs: can mimic B12/
Folate deticiencies.
• Bi-lobed neutrophils.
Myelodysplasia
& Serum B12
•个Hcy
・↑ MMA
• Red tongue
B12 deficiency
(malabsorption, increased need, no proteases, decreased stomach acid, Crohn's/celiac)

Anemia: differential diagnosis

Primary Amenorrhea Differential Diagnosis*
> 15 years no menarche and present 2° sexual characteristics
OR
> 13 years no menarche and absent 2° sexual characteristics
History and Examination
B-HCG, TSH and PRL
HCG T
TSH 1 or t
All normal
Evaluate for
Thyroid disorders
Breast Tanner Staging
Poor breast development
Good breast development
Estrogen is present
The ovaries are present and functioning (exclude AIS)
Pelvic US
Investigation
Result
• Diagnosis
• Category
C Est. Prevalence
DDx
Pregnancy
Tumor
Estrogen is absent or non-functioning
FSH, LH
Check if the problem is with the ovaries or elsewhere in the axis
FSH, LH T
FSH, LH D
† Hypergonadotropic
‡ Hypogonadism
The ovaries are failing to secrete estrogen and causing the problem
† Hypogonadotropic
+ Hypogonadism
The pituitary gland or somewhere up the axis are causing the problem
DDx
Turner Syndrome
DDx
Delayed puberty
Premature
Ovarian Failure
HPA axis dysfunction
Kallman Syndrome
Designed by Khudhur M.
Est.
14%
Est.
14%
Uterus absent -
Karyotype
46.XX
46,XY
Probable Dx
Probable Dx
Mullerian agenesis
Androgen insensitivity S.
Estrogen level is normal in these patients. also named
MRKH Syndrome.
High levels of testosterone are aromatized to estrogen
Uterus present +
Outflow tract
Obstructed
Intact +
DDx
Imperforate Hyman
Evaluate for 2°
Amenorrhea
Transverse Vaginal
Septum
Est.
3%

Primary Amenorrhea: differential diagnosis

Approach to Hypoglycemia
(2) Presentation
• Asymptomatic
• Autonomic (anxiety, pallor, Sweaty, tachycardia, tremor, hunger)
• Neuroglycopenic (confusion, DLOC, stroke-like, coma, death)
(3) Evaluation
With DM: fingerstick glucose (if unavailable, suspicion is enough to start Ix)
Without DM: fingerstick glucose,
Insulin, C-peptide, oral hypoglycemic screen
Don't delay!
"Action" to look for
(4) Action
Conscious?
Unconscious?
Able to eat
Unable to eat
Treat Orally
1. 5-20g glucose
(honey, orange juice)
2. Followed by long-acting CHO (slice of bread, snack)
Has IV Access
Treat IV
1. 10-25g glucose (20-
2. 50cc of D50W over
2min) - can be
repeated every 15min as needed
3. Followed by D10W
maintenance of 6-9 mg/kg/min (250-
375 cc per hour for a minimum of 4 hours)
MADE WITH MEDGRAM.NET
(5) Monitor
1. After 15min of each bolus: until RBS > 80-
100mg
2. Every 30 mins: next 2
hours
3. Every hour: as long as the cause needs (minimally 4hrs)
No IV Access
Treat IM / SubQ
Glucagon 1mg
Followed by Oral or I.V. maintenance immediately
No glucagon?
NG-tube, Candy gel in oral vestibule, Rectal or intranasal D50W (not based on guidelines)

Hypoglycemia: management

Jaundice Differential Diagnosis*
Measure bilirubin
† Indirect bilirubin
† Direct bilirubin
Unconjucated B.
Impaired hepatic intake, hemolysis or defective conjucation
ー
CBC
Retic T
Retic t
+ ALT, AST
Hemolysis
RBCs are being destroyed →
excess bilirubin
Non-Hemolytic
There is an error in bilirubin conjucation
Hepatocellular
Injury
Hepatocytes are being destroyed and releasing ALT/AST
Next Steps
Blood film
Next Steps
Family Hx
ALT > AST
AST:ALT > 2
Viral serology
LFTs
Genetic studies
Next Steps
Viral serology
Possible diagnoses
Alcoholic Liver D.
ANA & ASMA
Hepatocellular ca
Possible diagnoses
G6PD
Possible diagnoses
Gilbert S.
AMA
Early Viral Hepatitis
Transferrins
Sickle Cell A.
AIHA
Crigler-Najjar S.
a1 antitrypsin
Neonatal Jaundice
МАНА
Possible diagnoses
Late Viral Hepatitis
* Please do not use commercially without permission. I hold no responsibility for the information presented here.
Acute Hepatic Injury
Toxins and Drugs
Conjucated B.
Hepatocellular injury, cholestasis or impaired excretion
LFT
rALP, GGT
Cholestasis
Bilirubin is being excreted in bile but is being trapped and is causing damage
Next Steps
Bile duct U/S
MRCP / ERCP
Possible diagnoses
Choledochlithiasis
Primary Sclerosing C.
Obstructing Tumors
Any liver disease
Pregnancy
Designed by Khudhur M.
khudhur_moh
了
me@khudhur.com
Normal
+ Excretion / Reuptake
of Bilirubin
Bilirubin is getting conjucated but trapped
Next Steps
Genetic studies
Histological studies
Family Hx
Possible diagnoses
Dubin-Johnson S.
Rotor S.

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