IV Fluids

A) Crystalloid solutions (< 30 000 Dalton):

1-Hypotonic solutions:

- D₅W, ½ NS, D5 ¼ NS, D5 ½ NS.

2-Isotonic solutions:

- NS, Ringer’s, Lactated Ringer’s (Hartmann’s), Ringer’s acetate.

3-Hypertonic solutions:

- NaCl (3%, 7.5%), Mannitol (10%, 20%), NaHCO₃ (5%, 7.5%, 8.4%).

B) Colloid solutions (> 30 000 Dalton):

1-Blood derived:

- Human albumin (5%, 25%).

- Plasma protein fraction 5%.

2-Synthetic:

a) Dextrose Starches:

- They are D-glucose polymers linked by alpha bonds into linear macromolecules prepared from sucrose.

- Their half-life is 12 hours.

- 6% Dextran-70 (Macrodex) MW = 70 000 Dalton

- 10% Dextran-40 (Rheomacrodex) MW = 40 000 Dalton

- Dextran-1 (Promit).

- Dose: 20 ml/kg/d., Max.: 1.5 L/d.

Disadvantages:

- Interfere with blood typing.

- Antiplatelet effect.

- Antigenic effect with anaphylactoid and anaphylactic reactions.

- Affect renal functions and can be associated with renal failure.

b) Gelatins:

- Their M.W. 30 000-35 000 Dalton.

- Their half-life is 4-5 hours.

- Succinylated Gelatin (Gelofusine 3.5%, 4%).

- Polygelline (Hemaccel 3.5%, Hemagel 4%).

- Dose: 20 ml/kg/d., Max.: 1.5 L/d.

Advantages:

- Does not interfere with blood grouping.

- Does not affect renal function.

Disadvantages:

- Histamine-mediated allergic reaction.

c) Hydroxy-Ethyl Starch (HES) (Etherified Starch):

Synthetic colloids resemble glycogen structurally, synthesized from amylopectin.

- Heta-starch (Hexa-starch) (e.g. HAES-Steril, Hespan): M.W. 450 000 Dalton, half-life 48 hours.

- Hextend: M.W. is higher, and the half-life is longer.

- Penta-starch: M.W. 200 000, half-life less than 24 hours.

- Tetra-starch: (e.g. Tetraspan, Voluven): M.W. 130 000, half-life less than 6 hours.

- Dose: 20-50 ml/kg/d.

Advantages:

- Do not affect the coagulation study.

- Not antigenic but can cause anaphylactoid reactions.

- Less expensive than human albumin.

Read More

Ovarian Hyperstimulation Syndrome (OHSS)

- It is a complication of some forms of fertility medication. Most cases are mild, but small proportions are severe.

Causative Medications:

- Associated with the injection of a hormone called human chorionic gonadotropin (hCG) which is used for inducing final oocyte maturation and/or triggering oocyte release.

- The risk is further increased by multiple doses of hCG after ovulation and if the procedure results in pregnancy.

- Using a gonadotropin-releasing hormone (GnRH) agonist instead of hCG for inducing final oocyte maturation and/or release results in an elimination of the risk of OHSS, but a slight decrease of the delivery rate of approximately 6%.

Epidemiology:

- Sporadic OHSS is very rare and may have a genetic component.

- Clomifene citrate therapy can occasionally lead to OHSS, but the vast majority of cases develop after the use of gonadotropin therapy (with the administration of FSH), (Menopur, Pergonal, Repronex) and administration of hCG to induce final oocyte maturation and/or trigger oocyte release, often in conjunction with in vitro fertilization (IVF).

- The frequency varies and depends on patient factors, management, and methods of surveillance. About 5% of treated patients may encounter moderate to severe OHSS.

- Mortality is low, but several fatal cases have been reported.

Risk Factors:

- Risk factors include young age, the development of many ovarian follicles under-stimulation, extremely elevated serum estradiol concentrations, the use of hCG for final oocyte maturation and/or release, the continued use of hCG for luteal support, and the occurrence of a pregnancy (resulting in hCG production).

Pathophysiology:

- OHSS has been characterized by the presence of multiple luteinized cysts within the ovaries leading to ovarian enlargement and secondary complications.

- The central feature of clinically significant OHSS is the development of vascular hyperpermeability and the resulting shift of fluids into the third space.

- As hCG causes the ovary to undergo extensive luteinization, large amounts of estrogens, progesterone, and local cytokines are released. It is almost certain that vascular endothelial growth factor (VEGF) is a key substance that induces vascular hyperpermeability, making local capillaries "leaky", leading to a shift of fluids from the intravascular system to the abdominal and pleural cavity.

- Supraphysiologic production of VEGF from many follicles under the prolonged effect of hCG appears to be the specific key process underlying OHSS. Thus, while the patient accumulates fluid in the third space, primarily in the form of ascites, she actually becomes hypovolemic and is at risk for respiratory, circulatory, and renal problems. Patients who are pregnant sustain the ovarian luteinization process through the production of hCG.

- Avoiding OHSS typically requires interrupting the pathological sequence, such as avoiding the use of hCG. One alternative is to use a GnRH agonist instead of hCG.

Classification:

Mild OHSS:

- The ovaries are enlarged (5–12 cm), slight weight gain, mild abdominal distension, abdominal pain, nausea, diarrhea, and there may be an accumulation of ascites.

Moderate OHSS:

- Excessive weight gain (> 2 pounds/day or > 1 kg/day), increased abdominal girth, vomiting, darker urine and oliguria, excessive thirst, and dry skin and/or hair (in addition to mild symptoms).

Severe OHSS:

- Marked abdominal distention, lower abdominal pains, darker urine or anuria, pleural effusion, respiratory distress, calf and chest pains. There may be hemoconcentration, and thrombosis (in addition to mild and moderate symptoms).

- Symptoms generally resolve in 1 to 2 weeks but will be more severe and persist longer if pregnancy occurs. This is due to hCG from the pregnancy acting on the corpus luteum in the ovaries in sustaining the pregnancy before the placenta has fully developed. Typically, even in severe OHSS with a developing pregnancy, the duration does not exceed the first trimester.

- Early OHSS develops before pregnancy testing and late OHSS is seen in early pregnancy.

Criteria for Severe OHSS:

- Enlarged ovary, ascites.
- Hematocrit > 45%, WBC > 15,000/microliter.

- Oliguria, creatinine 1.0-1.5 mg/dL, creatinine clearance > 50 ml/min.

- Liver dysfunction, anasarca (extreme generalized edema).

Critical OHSS:

- Enlarged ovary, tense ascites with hydrothorax and pericardial effusion.

- Hematocrit > 55%, WBC > 25,000/microliter.

- Oligoanuria, creatinine > 1.6 mg/dL, creatinine clearance < 50 mL/min.

- Renal failure, thromboembolic phenomena (DVT, PE), ARDS.

Complications:

- Ovarian torsion, ovarian rupture, thrombophlebitis, and renal insufficiency.

Prevention:

- Physicians can reduce the risk of OHSS by monitoring FSH therapy, and by withholding hCG medication.

- Regarding dopamine agonists as prophylaxis, a systematic review and meta-analysis concluded that prophylactic treatment with Cabergoline (Dostinex) reduces the incidence, but not the severity of OHSS, without compromising pregnancy outcomes.

- OHSS may also be prevented by coasting, which is ovarian hyperstimulation in IVF without hCG administration for final maturation of follicles.

Treatment:

Mild OHSS:

- Can be treated conservatively with monitoring of abdominal girth, weight, and discomfort on an outpatient basis until either conception or menstruation occurs. Conception can cause mild OHSS to worsen in severity.

Moderate OHSS:

- Is treated with bed rest, fluids (IV hydration), and close monitoring of labs such as electrolytes (hyponatremia, hyperkalemia, acidosis), blood counts, and coagulation profile (PT, aPTT, INR). Ultrasound may be used to monitor the size of ovarian follicles. Depending on the situation, a physician may closely monitor a patient's fluid intake and output on an outpatient basis, looking for an increased discrepancy in fluid balance (over 1-liter discrepancy is cause for concern). Resolution of the syndrome is measured by decreasing the size of the follicular cysts on 2 consecutive ultrasounds.

Severe OHSS:

- Aspiration of accumulated fluid (ascites) from the abdominal (paracentesis) / pleural cavity may be necessary, intercostal tube, as well as opioids for the pain.

- If the OHSS develops within an IVF protocol, it can be prudent to postpone the transfer of the pre-embryos since the establishment of pregnancy can lengthen the recovery time or contribute to a more severe course. 

Read More

Ebstein’s Anomaly

-A rare congenital cardiac abnormality.

-The septal and posterior cusps of the tricuspid valve are displaced downwards and are elongated, such that a varying amount of the right ventricle effectively forms part of the atrium. Its wall is thin and it contracts poorly. The remaining functional part of the right ventricle is therefore small.

-The foramen ovale is patent, or defective, in 80% of cases.

-The degree of abnormality of right ventricular function, and the size of the ASD, are probably the main determinants of the severity of the condition, which varies considerably.

-The right ventricular systolic pressure is low, and the RVEDP is elevated. Tricuspid incompetence can occur.

-There may be a right to left shunt, with cyanosis, on effort, and pulmonary hypertension and right heart failure may supervene.

-The natural history of the disease is very variable. Fifty percent of cases present in infancy with cyanosis, and 42% die in the first 6 weeks of life.

-In those who survive to adulthood, symptoms may be precipitated by the onset of arrhythmias, or by pregnancy. A few patients remain asymptomatic, even as adults, although once symptoms develop, the disability can increase rapidly.

-A cardiothoracic ratio of ≥ 0.65 is a better predictor of sudden death than the symptomatic state, and those who developed atrial fibrillation died within 5 years. It has therefore been suggested that tricuspid surgery should be undertaken before the cardiothoracic ratio reaches 0.65.

Preoperative Abnormalities:

1. There may be a right to left shunt, with dyspnea and cyanosis at rest, or on moderate exertion. Alternatively, the patient may be asymptomatic.

2. Episodes of tachyarrhythmias occur in 25% of patients. Some provoke syncopal attacks.

3. The ECG may show varying abnormalities, including large peaked P waves, a long P–R interval, Wolff–Parkinson–White syndrome, RBBB, and right heart strain. Paroxysmal supraventricular tachycardia occurs in 15%, usually because of the presence of WPW syndrome.

4. Chest X-ray may show cardiomegaly, with a prominent right heart border, and poorly perfused lung fields.

5. Paradoxical systemic embolism and bacterial endocarditis may occur.

6. Many other lesions of the tricuspid valve or right ventricle may mimic Ebstein’s anomaly, therefore the discriminating clinical and echocardiographic features for correct diagnosis have been enumerated.

Anesthetic Problems:

These will depend upon the anatomical abnormality, the degree of right to left shunt, and the presence or absence of right heart failure.

1. Induction time is prolonged, because of the pooling of drugs in the large atrial chamber.

2. Intracardiac catheter insertion may be hazardous because it can provoke serious cardiac arrhythmias.

3. Air entering peripheral venous lines or any open veins at subatmospheric pressure may cause paradoxical air emboli.

4. Tachycardia is poorly tolerated because of impaired filling of the functionally small right ventricle.

5. Hypotension may increase the right to left shunt if present.

6. Hypoxia causes pulmonary vasoconstriction, which also increases a right to left shunt.

7. There is a risk of bacterial endocarditis, especially if a CVP line is in place.

8. Deterioration may occur in pregnancy because of a decrease in right ventricular function, and an increase in blood volume and cardiac output, or with the onset of arrhythmias.

Management:

1. The severity of the lesion must be assessed. In the presence of maternal cyanosis or arrhythmias during pregnancy, there should be close monitoring of both mother and fetus. Deterioration may occur, despite previous successful pregnancies.

2. Treatment of heart failure and arrhythmias.

3. Antibiotic prophylaxis against bacterial endocarditis.

4. If a CVP is used for monitoring, its tip should be kept within the superior vena cava. The use of intracardiac catheters should probably be avoided.

5. Techniques should aim to minimize tachycardia and hypotension.

6. Oxygen therapy increases pulmonary vasodilatation. Long-term maternal therapy is required during pregnancy from 14 weeks, to treat fetal hypoxia that is demonstrated by umbilical venous blood gases.

7. Several anesthetic techniques have been described. A two-catheter epidural technique can be used for vaginal delivery to minimize hypotension. Bupivacaine doses must be fractionated and saline rather than air used to site the epidural, to avoid paradoxical air emboli. Cesarean section under general anesthesia, preceded by fentanyl, and a neurolept analgesic technique for hysterectomy, have been described.

Read More

Acquired C1 Esterase Inhibitor Deficiency

-This may be a familial or, more rarely, an acquired disorder involving the complement system.

-The acquired form is mostly associated with a B-lymphocyte malignancy, and antibodies have been detected against abnormal immunoglobulins present on the malignant B-cells. The reaction between the two causes C1 activation, which in turn produces a secondary reduction in the concentrations of C1, C2, and C4 and reduced functional activity of the C1 esterase inhibitor.

-This form must be distinguished from the physical forms of angioedema that occur in response to food, drugs, or insect bites, or in association with connective tissue disorders.

-Recently, many patients have developed angioedema in response to treatment with ACE inhibitors, particularly enalapril and captopril. Substantial increases in plasma bradykinin have been demonstrated during attacks of hereditary, acquired, and captopril-induced angioneurotic edema.

Preoperative Abnormalities:

1. Intermittent attacks of angioneurotic edema that can involve any part of the body, and result from extravasation of intravascular fluid and protein into subcutaneous and mucosal structures.

2. As with hereditary angioneurotic edema, there is a low level of C1 esterase inhibitor, and sometimes life-threatening episodes of edema of the upper airway may develop in response to stress or local trauma, particularly dental treatment. However, attacks of edema may occur without any obvious reason, and recurrent abdominal pain may be a presenting feature.

3. As with the hereditary form, epinephrine (adrenaline), antihistamines, and steroids are ineffective for prophylaxis, and for treatment of these attacks.

4. The two conditions may be distinguished by the fact that in the acquired form the onset is late, no family history is elicited, no complement abnormalities are found in the patient’s blood relatives, and the underlying malignancy may already have been diagnosed.

5. Differentiation may now be made on measurement of the C1q subunit of C1; patients with acquired deficiency have a decreased level of C1q, compared with those with the hereditary form, in whom the C1 level is normal.

Anesthetic Problems:

1. Tracheal intubation and manipulation of the upper airway may precipitate local angioneurotic edema, for which treatment with epinephrine (adrenaline), steroids, and antihistamines is ineffective. Edema may also occur after dental extractions.

2. Although tranexamic acid has been recommended to prevent attacks in both forms, venous thrombosis has been reported after its prophylactic use during surgery in the acquired disease.

Management:

1. Progestogen derivatives: Increase the hepatic synthesis of a C1 esterase inhibitor. Its prophylactic value is acquired and hereditary disorders have been reported.

a) Danazol (200 mg TDS) should be given preoperatively but may take several days to become effective.

b) Stanozolol (0.5–8 mg/day) can also be used.

-The lower levels will be required for maintenance, whilst higher levels may be needed in the initial stages. A patient with autoimmune C1 EI, who was known to be carrying a male fetus, was given short-term therapy at 40 weeks of gestation.

2. Tranexamic acid: It should be avoided in the acquired form, especially in the presence of a thrombocytosis.

3. Fresh frozen plasma, and C1 esterase inhibitor concentrate: Used as preoperative prophylaxis and treatment.

Read more ☛ Angioneurotic Edema

Read More

Dexmedetomidine

Mechanism of Action:

-It is an imidazole derivative and is a specific alpha-2 adrenoceptor agonist that acts via post-synaptic alpha-2 receptors primarily in the locus ceruleus to increase conductance through K+ channels.

Uses and Dose:

-Its main actions are sedation, anxiolysis, and analgesia

-It is a clear, colorless isotonic solution containing 100 g/ml of dexmedetomidine base and 9 mg/ml of sodium chloride in water. The solution is preservative-free and contains no additives.

-Dexmedetomidine can be administered intravenously, intramuscularly, and transdermally.

1. ICU Sedation:

-Used for sedation of initially intubated and mechanically ventilated patients in ICU.

-Loading: 1 mcg/kg IV over 10 minutes; loading dose may not be required for adults converted from other sedative therapy.

-Maintenance 0.2-0.7 mcg/kg/h. continuous IV infusion; not to exceed 24 h.

-The duration of use should not exceed 24 hours.

-Dexmedetomidine has been infused in mechanically ventilated patients before, during, and after extubation; it is not necessary to discontinue dexmedetomidine before extubation.

2. Procedural Sedation:

Indicated for sedation of non-intubated patients before and/or during surgical and other procedures.

Loading: 1 mcg/kg IV over 10 minutes.

Maintenance 0.6 mcg/kg/h. IV titrate to effect (usually 0.2-1 mcg/kg/h.).

3. Awake Fiberoptic Intubation:

Loading: 1 mcg/kg IV over 10 minutes.

Maintenance 0.7 mcg/kg/hr IV until endotracheal tube secured.

Dosage Modifications:

-Dose reduction may be required if co-administered with other concomitant anesthetics, sedatives, hypnotics, or opioids.

-Consider dose reduction in patients with hepatic impairment or aged ≥ 65 y.; clearance decreases with increasing severity of hepatic impairment.

-Renal impairment: No dosage adjustment required.

Pharmacokinetics

Distribution: It is 94% protein-bound in the plasma; the volume of distribution is 1.33 l/kg. The distribution half-life is 6 minutes.

Metabolism: The drug undergoes extensive hepatic metabolism to methyl and glucuronide conjugates.

Excretion: 95% of the metabolites are excreted in the urine. The elimination half-life is 2 hours, and the clearance is 39 l/hour.

Pharmacodynamics:

1. Cardiovascular System: It causes a predictable decrease in the mean arterial pressure and heart rate.

2. Respiratory System: It causes a slight increase in PaCO₂ and a decrease in minute ventilation, with minimal change in the respiratory rate—these effects are not clinically significant.

3. Central Nervous System: The drug is sedative and anxiolytic—ventilated patients remain easily arousable and cooperative during treatment. Reversible memory impairment is an additional feature.

4. Metabolic / Other: It causes a decrease in plasma epinephrine and norepinephrine concentrations. It does not impair adrenal steroidogenesis when used in the short term.

Side Effects:

Hypotension, bradycardia, nausea, and a dry mouth are the most commonly reported side effects of the drug.

Read More

Angioneurotic Edema

-A general term applied to the development of acute edema in the subcutaneous or submucous tissues.

-Anesthetic help may be sought during an attack, when edema of the lips, tongue, or larynx may cause respiratory problems.

Causes:

-Angioedema may be secondary to the release of histamine, or many other vasoactive substances such as bradykinins, prostaglandins, or leukotrienes.

-It is thought that pediatric and adult angioedemas differ. Children are less likely to require intubation or tracheostomy than adults. Recent work in adults has shown substantial increases in plasma bradykinin during attacks of hereditary, acquired, or captopril-induced angioedema.

-The development of edema may be:

1. Part of a general anaphylactoid or anaphylactic reaction to a drug, bite, sting, or the ingestion of a substance.

2. A manifestation of hereditary angioneurotic edema, a condition caused by a deficiency of C1 esterase inhibitor.

3. A result of an acquired form of C1 esterase inhibitor deficiency which usually occurs in association with a B-lymphocyte malignancy.

4. A known side effect of a drug. Recently, there have been several cases of angioedema reported, usually involving the tongue, floor of the mouth, epiglottis, and aryepiglottic folds, secondary to treatment with ACE inhibitors. Most occur in the first week of treatment but may be delayed for up to a year. Can be associated with elevated serum bradykinin levels.

Presentation:

1. There may be a history of a predisposing factor. This can be ingestion of food or a drug, an infection, bite or sting, a family history of angioedema, or a B-lymphocytic malignancy.

2. Edema of subcutaneous tissue may occur alone or be accompanied by hypotension.

3. Patients taking ACE inhibitors have developed problems in the perioperative period. Angioedema of the tongue occurred 15 min after tracheal tube removal.

4. A patient with acquired C1 esterase inhibitor deficiency undergoing cardiopulmonary bypass had massive activation of the common pathway, coagulopathy, pulmonary edema, and circulatory collapse.

Management:

1. Assessment of severity of airway obstruction.

2. If the angioedema is part of an anaphylactic or anaphylactoid reaction:

a) Give epinephrine (adrenaline) IV or IM, 0.1–0.5 mg depending on the severity.

b) If the condition is severe and involves the glottis, an airway should be established, either by tracheal intubation, cricothyroidotomy, or tracheostomy.

c) Second-line treatment includes IV fluids, chlorpheniramine IV 10–20 mg, and steroids.

3. Hereditary angioneurotic edema, or acquired C1 esterase inhibitor deficiency. These do not respond to epinephrine (adrenaline) or antihistamines, but to replacement of the deficient inhibitor by either:

a) An infusion of fresh frozen plasma.

b) Purified C1 esterase inhibitor concentrate.

Read more ☛ Acquired C1 Esterase Inhibitor Deficiency

Read More

Jugular Venous Oximetry

Jugular Venous Oximetry (JVO)

-It provides insight into the metabolic and oxygenation state of the brain.

-It provides information about the balance of oxygen supply and demand, for a larger portion, if not the complete brain.

Indications:

-During cardiopulmonary bypass

-Neurosurgery

-After traumatic brain injury.

Figure 1: JVO Catheterization Technique

Technique:

-A catheter is inserted into the jugular vein in a retrograde fashion (using Seldinger’s technique) so that its tip sits at the base of the skull in the jugular bulb. This allows continuous pressure monitoring as well as intermittent withdrawal of a jugular venous blood sample for gas analysis (Fig. 1).

-Continuous monitoring: can be achieved using an oximetry catheter inserted via a conduit sheath.

-Confirmation of location: can be made with a lateral cervical spine x-ray (Fig. 2).

Figure 2: JVO Catheter Lateral Cervical Spine X-Ray 

Identification of the dominant Jugular vein:

For the best representation of the metabolic state of the brain, the catheter should be placed in the dominant jugular vein, most commonly the right side. Confirmed by:

-In patients who have had a cerebral angiogram, the venous phase of the study will provide information on dominant venous drainage.

-The intra-arterial contrast will drain almost exclusively through one jugular vein, regardless of the side of injection.

-Side dominance can also be predicted using ultrasound where the dominant vein may be larger. In the absence of this information, the right side is preferred.

The pressure gradient between the jugular venous pressure and the central venous pressure:

-Pressure transduction of the jugular bulb catheter allows comparison with the central venous pressure to rule out potential venous obstruction.

-In a supine patient with a neutral neck position, there should be no pressure gradient between the tip of the jugular bulb and the central venous catheter.

-Although rare, a significant gradient (> 4 mmHg) can occasionally develop during positioning if there is significant twisting or bending of the neck.

-This gradient indicates venous obstruction, potentially causing brain edema or ischemia.

-The head should be repositioned until the gradient resolves.

Interpretation of blood gas analysis of jugular venous blood sample:

-The saturation of jugular venous blood (SjvO₂) demonstrates whether cerebral blood flow (CBF) is sufficient to meet the cerebral metabolic rate for oxygen (CMRO₂) of the brain (Lower values of SjvO₂ reflecting greater uptake by the brain and therefore less blood flow).

-It is essential that blood samples from the retrograde catheter be drawn slowly to avoid contamination from non-cerebral venous blood.

-A normal value is between 65-75 %. Desaturation (SjvO₂ < 55 %) indicates impending cerebral ischemia (e.g., caused by hypotension, hypocapnia, increasing cerebral edema).

-In traumatic brain injury, SjvO₂ below 50% for more than 10 min. is undesirable and associated with poor outcomes. However, it has low sensitivity, (a relatively large volume of tissue must be affected, approximately 13 % before SjvO₂ levels decreased below 50 %).

-Intraoperative hyperventilation will lower SjvO₂ as it decreases CBF.

-In the setting of a non-traumatized brain that is exposed to moderate hyperventilation for the duration of a neurosurgical procedure, the acceptable level for SjvO₂ is unknown.

-In the absence of other demands, it is reasonable to guide intraoperative hyperventilation by maintaining SjvO₂ > 50%.

-Measurement of simultaneous arterial and jugular venous samples allows the determination of lactate output from the brain, the presence of which indicates the occurrence of anaerobic metabolism.

Disadvantages & Limitations:

-It is a global monitor that could easily miss small areas of regional ischemia.

-If CBF & O₂ consumption both decreased (e.g., in severe brain injury, SjvO₂ may be unchanged.

Read More