INVOS™: In Vivo Optical Spectroscopy

Overview:

➧ INVOS™ system technology gives a noninvasive “window” to the body’s microvasculature; a direct and dynamic site of gas exchange that transports about half the body’s blood volume. 

➧ Measuring blood oxygenation in the microvasculature results in sensitive and site-specific insights on perfusion adequacy and multi-sensor monitoring gives data about perfusion distribution across the brain and body. 

➧ The non-invasive INVOS System reports the venous-weighted regional hemoglobin oxygen saturation (rSO₂) in the tissue under the sensor; reflecting the Hb bound O₂ remaining after tissues have taken what they need. Decreases in this venous reserve indicate increased ischemic risk and compromised tissue perfusion.

Clinical applications:

-Cerebral application: Brain area measurement

-Somatic application: Tissue area of measurement

Principle:

➧ The INVOS™ system utilizes near-infrared light at wavelengths that are absorbed by hemoglobin (730 and 810 nm). Light travels from the sensor’s light-emitting diode to either a proximal or distal detector, permitting separate data processing of shallow and deep optical signals.

➧ INVOS™ system’s ability to localize the area of measurement, called the spatial resolution, has been empirically validated in human subjects.

➧ Data from the scalp and surface tissue are subtracted and suppressed, reflecting rSO₂ in deeper tissues. This same concept applies to somatic monitoring.

➧ The result is continuous, real-time adequacy of perfusion data in up to four sites of your choice.

Clinical characteristics:

1-Noninvasive 

2-Continuous, real-time

3-Capillary (Venous and Arterial) sample

4-Measures the balance between O₂ supply and demand beneath the sensor

5-End organ oxygenation and perfusion

6-Requires neither pulsatility nor blood flow

Interpretation Values:

1-Cerebral: High blood flow, High O₂ extraction: 

➧ Typical rSO₂ range: 60-80%; assuming SpO₂ is > 90%.

➧ Common intervention trigger: rSO₂ < 50% or 20% change from rSO₂ baseline.

➧ Critical threshold: rSO₂ < 45% or 25% change from rSO₂ baseline.

2-Somatic: Variable blood flow, Lower O₂ extraction:

➧ Variances in the cerebral-somatic relationship may be indicative of pathology. 

➧ Watch for drops of 20% below patient baseline. 

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Acute Kidney Injury Biomarkers

Acute Kidney Injury Biomarkers

I) Functional markers

1-Serum Creatinine (SCr):

➧ It is a degradation product of muscle cells and represents a surrogate for the efficiency of glomerular filtration.

➧ It has poor predictive accuracy for renal injury, particularly, in the early stages of AKI.

➧ In the case of critical illness, SCr concentrations are subject to large fluctuations due to a patient’s induced dilutional volume status, the catabolic effects of critical illness, the likelihood of concentration decreases in septic conditions, and the increased tubular excretion with diminishing the renal function.

➧ Furthermore, after an injurious event, the rise in SCr is slow.

➧ Therefore, detection of the earliest evidence of AKI necessitates the use of other plasma or urinary biomarkers.

2-Plasma/Serum Cystatin C (CyC):

➧ It is a 13-kDa, non-glycosylated, cysteine protease inhibitor produced by all nucleated cells at a constant rate.

➧ In healthy subjects, plasma CyC (pCyC) is excreted through glomerular filtration and metabolized completely by the proximal tubules. There is no evident tubular secretion (not detectable in urine in healthy subjects).

➧ Several studies claim the superiority of pCyC against SCr to detect minor reductions in glomerular filtration rate (GFR).

➧ It is detected in plasma and urine 12-24 h. post-renal injury.

Confounding factors: older age, Gender, Weight, Height, Systemic inflammation, High levels of C-reactive protein, Malignancy, Thyroid disorders, immunosuppressive therapy, Glucocorticoid deficiency or excess, and Smoking.

3-Fractional Excretion of sodium (FENa):

➧ (FENa) measures the percent of filtered sodium that is excreted in the urine.

➧ This calculation is widely used to help differentiate prerenal disease (decreased renal perfusion) from acute tubular necrosis (ATN) as the cause of AKI.

➧ In pre-renal azotemia, the proximal tubules reabsorb filtered sodium resulting in a very low urine sodium concentration (<20 mmol/L) and FENa is <1%.

➧ In intrinsic AKI the urine sodium concentration is >40 mmol/L and FENa is >1%.

4- Proenkephalin A (Penkid):

➧ Penkid is a 5-kDa, stable breakdown product of enkephalins.

➧ It accumulates in the blood in settings of reduced GFR.

➧ It is associated with AKI and mortality in patients with sepsis and heart failure.

II) Low-molecular-weight proteins

1-Urine Cystatin C (uCyC):

➧ The urinary excretion of CyC (uCyC) specifically reflects tubular damage because systemically produced cystatin C is normally not found in urine.

2-Urine α1/β2 microglobulin:

III) Up-regulated proteins

1-Kidney Injury Molecule-1 (KIM-1) (Cytoprotection):

➧ It is a type I transmembrane glycoprotein with a cleavable ectodomain (90-kDa).

➧ It is localized in the apical membrane of dilated tubules in an acute and chronic injury.

➧ It is produced by proximal tubular cells after ischemic or nephrotoxic injury; no systemic source.

➧ KIM-1 plays a role in regeneration processes after epithelial injury and in the removal of dead cells in the tubular lumen through phagocytosis.

➧ A reduction in proteinuria with renin-angiotensin-aldosterone blockade is accompanied by a reduction in urinary KIM-1 excretion.

➧ It is detected in urine 12-24 h. after renal injury

Confounding factors: Renal cell carcinoma, Chronic proteinuria, Chronic kidney disease, Sickle cell nephropathy.

2-Neutrophil Gelatinase-Associated Lipocalin (NGAL) (also known as oncogene 24p3) (Iron binding):

➧ It is a 25-kDa glycoprotein produced by epithelial tissues throughout the body.

➧ It is a small protein linked to neutrophil gelatinase in specific leukocyte granules.

➧ It is also expressed in a variety of epithelial tissues associated with anti-microbial defense.

➧ NGAL’s composite molecule binds ferric siderophores, induces epithelial growth, has protective effects in ischemia, and is up-regulated by systemic bacterial infections.

➧ Plasma NGAL is excreted via glomerular filtration and undergoes complete reabsorption in healthy tubular cells. It is also produced in distal tubular segments.

➧ It is detected in plasma and urine 2-4 h. after AKI.

Confounding factors: Malignancy, Chronic kidney disease, Pancreatitis, COPD, Endometrial hyperplasia.

3-Liver Fatty Acid Binding Protein (L-FABP):

➧ They are small (15-kDa) cytoplasmic proteins (intracellular lipid chaperones) produced in tissues with active fatty acid metabolism (liver, intestine, pancreas, lung, nervous system, stomach, and proximal tubular cells).

➧ Their primary function is the facilitation of long-chain fatty acid transport, the regulation of gene expression, and the reduction of oxidative stress.

➧ Urinary (L-FABP) is undetectable in healthy control urine, which is explained by efficient proximal tubular internalization via megalin-mediated endocytosis.

➧ Under ischemic conditions, tubular L-FABP gene expression is induced. L-FABP is freely filtered in glomeruli and reabsorbed in proximal tubular cells; increasing urinary excretion after tubular cell damage.

➧ In renal disease, the proximal tubular re-absorption of L-FABP is reduced.

➧ Detected in plasma and urine 1 h. after ischemic tubular injury.

Confounding factors: Chronic kidney disease, Polycystic kidney disease, Liver disease, Sepsis.

4-Interleukin-18 (IL-18):

➧ It is 18-kDa pro-inflammatory cytokine, released from proximal tubular cells following injury.

➧ Detected in plasma and urine 6-24 h. after renal injury

Confounding factors: Inflammation, Heart failure, Sepsis.

5-Tissue Inhibitor of Metallo-Proteinases-2 (TIMP-2):

6-Insulin-like Growth Factor Binding Protein-7 (IGFBP-7):

➧ They are cell cycle arrest proteins that have been suggested as early indicators of AKI.

➧ In particular, urinary (TIMP-2) and (IGFBP-7) are biomarkers of the G1 renal tubular cell cycle arrest at the early phase of AKI.

➧ The product of the urinary concentrations of TIMP-2 and IGFBP-7 (urinary [TIMP-2] × [IGFBP-7]) is a promising biomarker for the early prediction of AKI.

IV) Tubular enzymes

1-Alpha-Glutathione-s-Transferase (α-GST):

2-Pi-Glutathione-s-Transferase (π-GST):

➧ (α-GST) and (π-GST) are 47-to 51-kDa cytoplasmic enzymes.

➧ They are both members of a multigene family of detoxification enzymes present in many organs including the kidney.

➧ Distribution across the entire nephron of structurally and functionally distinct isoforms has been demonstrated.

➧ In urine, these enzymes are normally not present.

➧ After the injury, α-GST is primarily detected in the proximal cells, whereas π-GST is observed in the distal parts.

➧ They are detected in urine 12 h. after AKI.

3-Gamma-Glutamyl Transpeptidase (GGT):

4-Alkaline Phosphatase (AP):

5-Alanine Amino-Peptidase (AAP):

➧ They are tubular brush border enzymes.

➧ They are released into the urine when there has been significant damage to the brush border membrane with loss of the microvillus structures.

6-N-Acetyl-β-D-Glucosaminidase (NAG):

➧ N-Acetyl-β-D-Glucosaminidase (NAG) is a lysosomal enzyme (>130-kDa) that is localized in the renal tubules.

➧ It precludes glomerular filtration (due to large MW), implying that urinary elevations have a tubular origin.

➧ Increased activity suggests injury to its cells but may also reflect increased lysosomal activity without cell disruption.

➧ NAG catalyzes the hydrolysis of terminal glucose residues in glycoproteins.

➧ It is detected in plasma and urine 12 h. after AKI

Confounding factors: Diabetic nephropathy.

V) Others

1-Retinol Binding Protein (RBP):

➧ It is 21-kDa single-chain glycoprotein; a specific carrier for retinol in the blood (delivers retinol from the liver to peripheral tissues).

➧ It is totally filtered by the glomeruli and reabsorbed but not secreted by proximal tubules; a minor decrease in tubular function leads to the excretion of RBP in urine.

➧ It is detected in plasma and urine

Confounding factors: Type II DM, Obesity, Acute critical illness.

2-Hepcidin:

➧ It is a 2.78-kDa peptide hormone predominantly produced in hepatocytes; some production in the kidney, heart, and brain.

➧ It is freely filtered with significant tubular uptake and catabolism (fractional excretion 2%).

➧ It is detected in plasma and urine after AKI.

Confounding factors: Systemic inflammation.

3-Hepatocyte Growth Factor (HGF):

➧ It is overexpressed after AKI.

➧ It is a marker linked to renal tubular epithelial cell regeneration.

4-Netrin-1:

➧ It is a laminin-related molecule, minimally expressed in proximal tubular epithelial cells of normal kidneys.

➧ It is highly expressed in injured proximal tubules.

➧ It is detected in urine after AKI.

5-Monocyte Chemo-attractant Peptide-1 (MCP-1):

➧ It is a peptide expressed in renal mesangial cells and podocytes.

➧ It is detected in urine after AKI.

Confounding factors: Variety of primary renal diseases.

6-Calprotectin:

➧ The calcium-binding complex of two proteins of the S100 group (S100A8/ S100A9).

➧ Derived from neutrophils and monocytes.

➧ Acts as an activator of the innate immune system.

➧ It is a measure of local inflammatory activity. It is detected in urine in intrinsic AKI.

Confounding factors: Inflammatory bowel disease, Urinary tract infection, Probably CKD.

7-MicroRNA:

➧ MicroRNAs are short, non-protein-coding RNA molecules between 19 and 25 nucleotides in length.

➧ They are epigenetic regulators of gene expression at the post-transcriptional level in response to kidney injury through messenger RNA (mRNA) signal repression.

➧ As key regulators of homeostasis, their dysregulation underlies several morbidities including kidney disease.

➧ MicroRNAs are used as diagnostic and prognostic biomarkers in AKI.

8- Chitinase-3-like protein 1 (CHI3L1) (YKL-40, HC-gp39):

➧ YKL-40 is a 40-kDa heparin- and chitin-binding glycoprotein also known as Human Cartilage glycoprotein 39 (HC-gp39), 38-kDa heparin-binding glycoprotein or chitinase-3-like protein 1 (CHI3L1).

➧ The abbreviation YKL-40 is based on the one-letter code for the first three N-terminal amino acids, tyrosine (Y), lysine (K), and leucine (L), and the apparent molecular weight of YKL-40.

➧ It plays an important role in AKI and repair.

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Bronchoscopy in ICU

Indications:

A) Diagnostic:

1-Investigation of an infectious process:

➧ Bronchoscopy and broncho-alveolar lavage (BAL) are commonly used for the identification of pathogens in the lower airways in the following circumstances: 

a) When it is not clear whether the presence of organisms represents infection or colonization. 

b) When the infection is caused by organisms that show a predilection for the peripheral airways (e.g. Pneumocystis jirovesii). 

c) When the infection is confined in a particular area of the lung (tuberculous and non-tuberculous mycobacteria as well as several fungal and opportunistic organisms).

2-Abnormal breath sounds:

➧ Abnormal breath sounds include: stridor, wheezes, or a combination of both and they are the most common indication of FOB in the NICU.

➧ In neonates, abnormal breath sounds are due to congenital abnormalities of the upper or lower airways.

➧ In older infants and children the causes are often iatrogenic (e.g. subglottic stenosis due to prolonged intubation, injury of the vocal cords, or recurrent laryngeal nerve causing paresis or paralysis).

3-Evaluation of the nature of abnormalities:

➧ Patients in the ICU often present with radiographic findings and/or symptoms of unclear etiology, e.g.: an airway filled with secretions can look radiographically identical to a completely compressed airway.

4-Others:

➧ Pneumonia, Trauma, Inhalation injury and burns, Tracheoesophageal fistula.

B) Therapeutic:

1-Placement of the endotracheal tube:

➧ The use of FOB for the placement of the endotracheal tube is reserved for cases in which high precision is required.

➧ e.g. placement of the ETT just above the carina in patients with very severe tracheomalacia; or selective intubation of one lung), or when congenital anatomical abnormalities or injuries preclude the proper opening of the jaw for direct laryngoscopy.

2-Placement of double-lumen ETT and confirmation of position

3-Extubation over FOB

4-Persistent or recurrent atelectasis

➧ Atelectasis is a major cause of clinical deterioration and/or of delay in the patients’ recovery, resulting from many causes such as; mucous plug, compression of the airways, alveolar destruction, and collapse.

5-Foreign body removal

6-Strictures and stenosis

7-Hemoptysis

Contraindications:

1-Full stomach

2-Bronchial asthma

3-Severe pulmonary hypertension

4-Tuberculosis

5-Acute myocardial infarction or unstable angina

6-Coagulopathy

Complications:

1-Increase HR, Bl. P, ICP, IOP

2-Laryngospasm and bronchospasm

3-Hypoxemia

4-Arrhythmia

5-Bleeding

6-Post-bronchoscopy fever

7-Pulmonary infiltrate

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Diabetic Ketoacidosis (DKA)

Physiology:

Hyperglycemia:

➧ Increased hepatic production of glucose.

➧ Diminished glucose uptake by peripheral tissues.

➧ Insulinopenia / Hyperglucagonemia.

Ketoacidemia:

➧ The ketoacid is acetoacetic acid. The byproduct is acetone. The non-keto-acid is beta-hydroxybutyric acid.

➧ Increased lipolysis and hepatic ketogenesis

➧ Reduced ketolysis by insulin-deficient peripheral tissues.

Fluid and Electrolyte Depletion:

➧ Osmotic diuresis and dehydration due to hyperglycemia.

➧ On average, water deficit is about 5L, sodium 500 mmol, potassium 400 mmol, and chloride 400 mmol.

General Considerations:

➤ Initial presentation of Type I DM (Can also occur in Type II DM).

➤ Increased insulin requirements in Type I DM (Infection, Trauma, Myocardial infarction, Surgery).

➤ Mortality is 5% in patients under 40 y. Up to 20% of the elderly.

➤ Estimates of 5-8 episodes per 1000 at-risk diabetics annually.

➤ One of the more common serious complications of insulin pump users – occurs 1 per 80 months of treatment. Typically due to unrecognized pump failure.

➤ Essentials of Diagnosis:

➧ Acidosis with pH < 7.3.

➧ Serum bicarbonate < 15 .mEq/L.

➧ The serum is positive for ketones.

➧ Elevated anion gap (variable, may occur without gap).

➧ Hyperglycemia > 250 mg/dL (no correlation between the severity of hyperglycemia and severity of ketoacidosis).

Clinical picture:

Symptoms:

➧ Early: Polyuria, Polydipsia, Fatigue, N/V.

➧ Late: Stupor – Coma.

Signs:

➧ Rapid, Deep Breathing.

➧ Fruity breath odor of acetone.

➧ Tachycardia, Hypotension, mild Hypothermia.

➧ Abdominal Pain and Tenderness.

Laboratory Findings:

➧ Glycosuria 4+, Ketonuria.

➧ Hyperglycemia, Ketonemia, Low arterial blood pH, and Low plasma bicarbonate.

➧ Elevated serum potassium (despite total body potassium depletion).

➧ Elevated serum amylase (not specific for pancreatitis in this setting, use lipase).

➧ Leukocytosis.

➧ If hyperthermic, likely due to infection since pts with DKA are hypothermic if uninfected.

Management of DKA:

Insulin Replacement:

➧ Regular Insulin IV bolus 0.1-0.2 units/kg to ‘prime’ insulin receptors.

➧ Regular Insulin infusion at 0.1 units/kg/h.

➧ Then replaced with SC regular insulin when hyperglycemia and ketoacidosis are controlled.

➧ Then oral intake + SC intermediate-acting insulin.

Fluid Replacement:

➧ The typical deficit is 4-5 L.

➧ Initially, NS 1 L/h. x 2 h., then 0.5 L/h. x 1-2 h., then 200-300 mL/h. till correction.

➧ Switch to ½ NS if serum Na > 150 mEq/L. 

➧ Add D5W if the glucose falls below 250 mg/dL, to maintain serum glucose 250-300 mg/dL to prevent hypoglycemia and cerebral edema.

Sodium Bicarbonate:

➧ 50 mmol

➧ Clinical benefit has not been demonstrated.

➧ Use to correct pH < 7, target pH of 7-7.2.

Potassium:

➧ 10-30 mEq/h. replacement to be started during the second or third hour of treatment.

Phosphate:

➧ Replete hypophosphatemia of < 1 mg/dL.

➧ 15 mmol K or Na phosphate in 100 mL saline.

➧ Replete slowly (3-4 mmol/h.) to avoid hypocalcemic tetany.

Treatment of Associated Infection:

➧ Antibiotics: as indicated.

➧ Cholecystitis and pyelonephritis may be particularly severe in these patients.

Read more ☛ Hypoglycemic Coma

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Hypoglycemic Coma

Hypoglycemia in Type I DM:

➧ Common in patients intensively controlled with insulin.

➧ Asymptomatic blood glucose levels of < 50 mg/dL occur daily in up to 56% of patients.

➧ Symptomatic hypoglycemia occurs 2X/week on average.

Severe Hypoglycemia:

➧ An episode requires intervention by another person for the patient to recover function.

Causes of Hypoglycemia in Diabetes:

➧ Delayed, reduced, or missed CHO intake.

➧ Increased glucose utilization (exercise).

➧ Decreased insulin clearance (renal failure).

➧ Alcohol -inhibits hepatic gluconeogenesis.

➧ Adrenal insufficiency or glucocorticoid dosage reduction.

Clinical picture:

Adrenergic:

➧ Tremor, anxiety, palpitations, hunger.

Neuroglycopenic:

➧ Dizziness, decreased concentration, blurred vision, tingling, lethargy.

Severe Hypoglycemia in Intensively Controlled Type I DM:

➧ Up to 25% yearly incidence.

➧ Disabling cognitive effects may take hours to fully resolve.

➧ May lead to seizures, and rarely, permanent neurological deficits.

➧ Estimated to be a causative factor in 4% of deaths.

Hypoglycemia Unawareness:

➧ Loss of autonomic warning symptoms of hypoglycemia.

➧ Occurs in 25-50% of patients with type I DM.

➧ Patients are no longer prompted to eat.

➧ Results in a 7X increased frequency of severe hypoglycemia.

Defective Glucose Counter-regulation in Type I DM:

➧ Reduced or absent glucagon response is common after 2-4 years.

➧ Deficient epinephrine response is common after 5-10 years.

➧ Results in a 25X increased frequency of severe hypoglycemia.

Hypoglycemia Unawareness and Defective Glucose Counter-regulation:

➧ Reversible by short-term avoidance of hypoglycemia.

Reduction of Hypoglycemia in Type I DM:

➧ Identify patients at increased risk:

- History of severe hypoglycemia.

- History of hypoglycemia unawareness.

- Normal or near-normal glycohemoglobin levels.

➧ Raise glycemic targets in the short term to regain symptom recognition.

➧ Education of patients and family members to recognize and treat hypoglycemia.

➧ Have unaware patients test blood glucose before performing a critical task (driving).

➧ Patients should have rapid-acting carbohydrates available at all times.

➧ Apply principles of intensive insulin therapy:

- Frequent home glucose monitoring.

- Flexible insulin regimens with dosage adjustments based on meal size, monitored blood glucose levels, and anticipated exercise.

➧ Replace insulin more physiologically:

- Multiple insulin injections.

- New ultra-short-acting insulin analogs: lispro, aspart, glulisine.

- Long-acting insulin analogs: glargine, detemir.

- Insulin pumps.

Subcutaneous, Continuous Glucose Monitors:

➧ Now available with alarms for high and low glucose readings.

➧ Useful for catching periods of hypoglycemia (especially overnight) of which patients are unaware.

➧ Shown to reduce the incidence of hypoglycemia in type I DM patients with prior severe hypoglycemia.

Management of Hypoglycemic Coma:

-If delayed, can cause permanent neurologic damage.

➧ 50% Dextrose in water: 50 ml IV over 3-5 min. followed by 5% dextrose in a water infusion.

➧ Glucagon: 0.5-1 mg IM/SC.

- Mobilizes hepatic glycogen stores.

➧ Hydrocortisone: for adrenal insufficiency.

➧ Hospitalize: those on sulfonylureas for 24 h.

Read more ☛ Diabetic Ketoacidosis (DKA)

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Acute Hypocalcemia

Causes:

1-Hypoparathyroidism

➧ Destruction of parathyroids (most commonly surgical – parathyroid resection or accidental).

➧ Acute hypomagnesemia

2-Reduced 1,25 (OH) vit D

3-Chronic renal insufficiency

➧ Acute systemic illness

➧ Drugs: ketoconazole, doxorubicin, cytarabine

➧ Increased uptake of Ca in bone

➧ Osteoblastic metastases

➧ Hungry bone syndrome

4-Complexing of Ca from the circulation

➧ ↑ albumin binding in alkalosis

➧ Acute pancreatitis with the formation of Ca soaps

➧ Transfusion-related citrate complexing

Clinical Picture:

Symptoms:

➧ Perioral numbness

➧ Tingling paresthesias

➧ Muscle cramps

➧ Carpopedal spasm

➧ Seizures

Signs:

➧ Hyperreflexia

➧ Chvostek's sign: (Figure 1, Figure 2)

(Tap on facial n. anterior to the earlobe or between the zygomatic arch and angle of the mouth → Unilateral spasm of facial muscles)

Figure 1: Chvostek's sign

Figure 2: Chvostek's sign

➧ Trousseau's sign: (Figure 3) 

(Inflate BP cuff 20 mmHg > SBP → Carpopedal spasm)

Figure 3: Trousseau's sign

➧ Hypotension

➧ Bradycardia

➧ Arrhythmias

➧ Prolonged QT interval (Figure 4)

Figure 4: Prolonged QT interval

ECG Changes: (Figure 5)

Figure 5: ECG changes in Acute Hypocalcemia

Biochemical Workup:

➧ S total Ca⁺², Albumin and Ionized Ca⁺² 

➧ S PO4⁺² 

➧ S Mg⁺² 

➧ Plasma PTH

- Low in hypoparathyroidism

- High in hungry bones syndrome

➧ 25 (OH)D3 and 1,25 (OH)D3 

➧ S. Amylase and Lipase

Management of Hypocalcemia:

1- First correct low Mg⁺²

2- Control of Tetany:

➧ Calcium gluconate: 10 ml of 10% solution IV over 5-10 min. and repeat as necessary in cases with frank generalized tetany.

➧ Slower continuous infusion of Calcium in less acute cases:

- 10% calcium chloride, 8 ml or 10% calcium gluconate, 22 ml in 100 ml isotonic saline over 10 min.-then continuous infusions of 1-2 mg/kg/h elemental calcium, lasting 6-12 h.; Oral daily maintenance 2-4 g.

- Vitamin D: 1-3 mg/d. oral.

3- Correction of alkalosis:

➧ Isotonic saline.

➧ Ammonium chloride: 2 g/4 h. oral to stop tetany.

Read more ☛ Acute Hypercalcemia

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