Anesthesia for Electroconvulsive Therapy

Principle:

-The exact mechanism of Electroconvulsive Therapy (ECT) is unknown. Electrical stimuli (electroconvulsive shock) are usually administered until a therapeutic generalized seizure is induced (30–60 sec. in duration).

-A good therapeutic effect is generally not achieved until a total of 400–700 seizures have been induced, in several sessions, over 2-3 weeks. Progressive short memory loss often occurs with an increasing number of treatments.

Physiological Effects:

-Seizure activity is characteristically associated with an “initial parasympathetic” discharge characterized by bradycardia and increased secretions. Marked bradycardia (<30 beats/min.) and even transient asystole (up to 6s) are occasionally seen.

-This is followed by “sustained sympathetic” discharge. Hypertension and tachycardia that follow are typically sustained for several minutes.

-Transient autonomic imbalance can produce arrhythmias and T-wave abnormalities on the ECG. Cerebral blood flow and ICP, intragastric pressure, and intraocular pressure all transiently increase.

Contraindications:

• Recent MI (<3 months)

• Recent stroke (usually <1 month)

• Intracranial mass or increased ICP from any cause

• More relative contraindications include:

- Angina

- Poorly controlled heart failure

- Significant pulmonary disease

-Bone fractures, Severe osteoporosis

- Pregnancy

- Glaucoma and retinal detachment.

Anesthetic Considerations:

-Amnesia is required only for the brief period (1–5 min) from when the NMB is given to when a therapeutic seizure has been successfully induced. The seizure itself usually results in a brief period of anterograde amnesia, somnolence, and often confusion. Consequently, only a short-acting induction agent is necessary.

-Increases in seizure threshold are often observed with each subsequent ECT.

-Most induction agents (Barbiturates, Benzodiazepines, and Propofol) have anticonvulsant properties, small doses must be used. The seizure threshold is increased and seizure duration is decreased by all of these agents.

--Sodium pentothal (2–4 mg/kg) was the first induction agent used, it raises the seizure threshold and decreases its duration.

--Methohexital (0.5-1.0 mg/kg): has been the induction agent of choice (gold standard) because it has very little effect on seizure duration and has a rapid onset and recovery profile. Unfortunately, methohexital is no longer available.

--Benzodiazepines: raise the seizure threshold and decrease its duration.

--Propofol (1–1.5 mg/kg): but higher doses reduce seizure duration.

--Etomidate (0.15-0.6 mg/kg): lacks anticonvulsant properties, increases seizure duration, and prolongs recovery.

--Ketamine (1.5-2 mg/kg): lacks anticonvulsant properties, and increases seizure duration, but is generally not used because it also increases the incidence of delayed awakening, nausea, and ataxia and is also associated with hallucinations during emergence.

-Short-acting opioids: are not given alone because they do not consistently produce amnesia.

-Sevoflurane (5%–8% for induction, followed by 1–2 MAC): is the only inhalational agent in widespread use for induction in ECT, with comparable effects to intravenous (IV) agents. It is preferred for patients not cooperative with IV access. It has the advantage of attenuating uterine contractions following ECT and is used in the third trimester of pregnancy.

-Induction agents in the descending order of seizure duration after their use are:

[Etomidate > Ketamine > Methohexital > Sevoflurane > Thiopental > Propofol]

-Induction agents in descending order of seizure threshold reducing property are:

[Etomidate > Ketamine > Methohexital > Thiopental > Propofol]

-Neuromuscular blockade: required from the time of electrical stimulation until the end of the seizure. A short-acting agent, such as succinylcholine (0.25–0.5 mg/kg), is most often selected.

-Ventilation: Controlled “mask ventilation” (with a backup plan of LMA if concerned about effective ventilation), is required until spontaneous respirations resume. As ECT is usually administered 3-times a week, repeated intubations may lead to airway trauma and edema. Hyperventilation can increase seizure duration and is routinely employed in some centers.

Monitoring:

-Routine monitoring should be as with the use of any other general anesthetic.

-Seizure activity is monitored by an unprocessed EEG. It can also be monitored in an isolated limb: a tourniquet is inflated around one arm before injection of succinylcholine, preventing entry of the NMB and allowing observation of convulsive motor activity in that arm.

Precautions:

-Rubber bite block: to avoid dental, tongue, and lips injury.

-Exaggerated parasympathetic effects: should be treated with atropine. In fact, premedication with glycopyrrolate is desirable both to prevent the profuse secretions associated with seizures and to attenuate bradycardia.

-Sympathetic manifestations: Nitroglycerin, Nifedipine, and α- and β-adrenergic blockers have all been employed successfully for control. High doses of β-adrenergic blockers (Esmolol, 200 mg), however, are reported to decrease seizure duration.

-Patients with pacemakers: may safely undergo ECT treatments, but a method to convert the pacemaker to a fixed mode, if necessary should be readily available.

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How to avoid ALI after Thoracic Surgery

How to avoid Acute Lung Injury (ALI) after Thoracic Surgery

-Fortunately, Acute Lung Injury (ALI) occurs infrequently, with an incidence of 2.5 % of all lung resections combined, and an incidence of 8% after pneumonectomy. However, when it occurs, ALI is associated with a risk of mortality or major morbidity of about 40%.

Causes of ALI:

I. Ventilated Lung:

1-Hyperoxia: (Oxygen toxicity, Reactive oxygen species)

2-Hyperperfusion: (Endothelial damage, Increased pulmonary vascular pressure)

3-Ventilatory Stress: (Volutrauma, Barotrauma, Atelectrauma)

II. Collapsed Lung:

1-OLV: (Ischemia/Reperfusion, Reexpansion, Cytokine release, Altered redox status)

2-Surgery: (Manipulation trauma, Lymphatic disruption)

III. Systemic:

-Cytokine release, Reactive oxygen species, Complement activation, Overhydration, Chemotherapy/Radiotherapy.

Prophylaxis against ALI:

A) Protective Lung Ventilation Strategies:

I. Lower Tidal Volumes (6–8 mL/kg):

-The use of lower tidal volumes may lead to lung derecruitment, atelectasis, and hypoxemia. Lung derecruitment may be avoided by the application of external PEEP and frequent recruitment maneuvers.

II. PEEP (5–10 cm H₂O):

-Although PEEP may prevent alveolar collapse and development of atelectasis, it may cause a decrease in PaO₂ due to diversion of blood flow away from the dependent, ventilated lung and an increase in the total shunt.

-Thus, PEEP must be customized to the underlying disease of each patient, and a new application of PEEP will rarely be the appropriate way to treat hypoxemia that occurs immediately after the onset of one-lung ventilation.

-Patients with obstructive pathology may develop intrinsic PEEP. In these patients, the application of external PEEP may lead to unpredictable levels of total PEEP.

III. Lower FiO₂ (50-80%):

-Although the management of one-lung ventilation has long included the use of 100% oxygen, evidence of oxygen toxicity has accumulated both experimentally and clinically.

-Clinicians recommend titrating FiO₂ to maintain the O₂ saturation >90%, especially in patients who have undergone adjuvant therapy and are at risk of developing ALI.

IV. Lower Ventilatory Pressures:

-Plateau pressure <25 cm H₂O; and peak airway pressure <35 cm H₂O, through the use of pressure-controlled ventilation, may diminish the risk of barotrauma.

-The flow pattern results in a more homogenous distribution of the tidal volume and improved dead space ventilation.

V. Permissive Hypercapnia:

-Periodic ABG analysis is helpful to ensure adequate ventilation. End-tidal CO₂ measurement may not be reliable due to increased dead space and an unpredictable gradient between the arterial and end-tidal CO₂ partial pressure.

VI. At the end of the procedure:

-The operative lung is inflated gradually to a peak inspiratory pressure of less than 30 cm H₂O to prevent disruption of the staple line.

-During reinflation of the operative lung, it may be helpful to clamp the lumen of the dependent lung, to limit over-distension.

B) IV Fluids:

-Restrict IV fluids in pulmonary resection to avoid lower lung syndrome (Gravity-dependent transudation of fluid).

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Cell (Blood) Salvage

Definition:

-Cell (blood) salvage is a process in which a patient’s own (lost) blood is collected, processed, and transfused back (‘Autologous’ blood transfusion), which is done by a cell saver machine.

Principle:

1-Collection of blood: blood is suctioned from the operative field, and then heparinized saline is added, filtered, and centrifuged to separate RBCs which are then washed.

2-Washing of RBCs: across a semi-permeable membrane to filter-out free Hb, plasma, WBCs, and platelets.

3-Re-transfusion: Washed RBCs are then suspended in saline (to achieve Hct of 60-70%) and transfused within 6 hours.

Advantages:

-Reduce or eliminate the need for ‘allogenic’ transfusion.

-‘Allogenic’ blood transfusion has been associated with an increased risk of postoperative infection, acute lung injury, perioperative MI, low CO HF, and tumor recurrence.

Indications:

-Anticipated blood loss >1L or >20% of estimated blood volume

-Patients with low Hb, multiple RBCs alloantibodies, rare blood group, and patient refusal of ‘allogenic’ blood transfusion

-Obstetrics: Controversial due to potential risk of amniotic fluid embolism. However; cell salvage with a Leucocyte-depletion filter (LDF) is considered safe

-Orthopedics: Reduce ‘allogenic’ transfusion & postoperative infection in arthroplasty

-Cardiac surgery: Leucocyte-depletion filter (LDF) use, reduce micro-emboli & lipid load of cell salvaged blood with an improvement of postoperative lung function.

-Vascular surgery

-Liver transplantation

-Jehovah’s Witness

Contraindications:

-Malignancy: due to risk of tumor dissemination

-Wound contamination: due to risk of systemic spread

-Old hemolyzed blood

-Use of collagen or hemostatic materials

-Obstetric surgery: due to risk of amniotic fluid embolism

-Ascites

Complications:

-Non-immune hemolysis: due to centrifugation

-Coagulopathy: due to large volumes of transfusion

-Citrate overdosage

-Air embolism

-Febrile non-hemolytic transfusion reaction

-Contamination: due to incomplete washing leading to contamination with drugs, activated leukocytes, cytokines, and microaggregates.

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Complications of Total Parenteral Nutrition (TPN)

I. Catheter-Related Complications:

-The hyperosmolarity of the dextrose and amino acid solutions requires infusion through large veins or central venous lines.

1-Misdirected Catheter: e.g., with subclavian vein cannulations – (mostly on the right) 10% resulted in misplacement of the catheter in the internal jugular vein.

2-Infection

3-Hematoma

4-Thrombosis

II. Carbohydrate Complications:

1-Hyperglycemia:

-Hyperglycemia is common during TPN; blood glucose levels >300 mg/dl were recorded in 20% of postoperative patients receiving TPN.

-A standard TPN regimen with 1,800 non-protein calories has ≈350 g of glucose, compared to 230 g in a standard tube feeding regimen.

-Tight glycemic control is not recommended in critically ill patients because of the risk of hypoglycemia, which has more serious consequences than hyperglycemia.

-The current recommendation for hospitalized patients is a target range of 140–180 mg% for blood glucose.

2-Insulin:

-If insulin therapy is required, regular insulin is preferred for critically ill patients, to prevent wide swings in glucose levels, by adding insulin to the TPN solutions.

-One shortcoming of IV insulin infusions is the propensity for insulin to adsorb to the plastic tubing in IV infusion sets. This affects the bioavailability of insulin but can be reduced by priming the IV infusion set with an insulin solution (e.g., 20 mL of saline containing 1unit/mL of regular insulin). But the priming procedure must be repeated each time the IV infusion set is changed.

-SC insulin can be used for stable patients. Regimens will vary in each patient, with a combination of intermediate or long-acting insulin with rapid-acting insulin, when needed.

3-Hypophosphatemia:

-The movement of glucose into cells is associated with a similar movement of phosphate into cells, and this provides phosphate for co-factors (e.g., thiamine pyrophosphate) that participate in glucose metabolism. This intracellular shift of phosphate can result in hypophosphatemia.

4-Hypokalemia:

-Glucose movement into cells is also accompanied by an intracellular shift of potassium (which is the basis for the use of glucose and insulin to treat severe hyperkalemia). This effect is usually transient, but continued glucose loading during TPN can lead to persistent hypokalemia.

5-Hypercapnia:

-Excess carbohydrate intake promotes CO₂ retention in patients with respiratory insufficiency. This was originally attributed to the high respiratory quotient (VCO₂/VO₂) associated with carbohydrate metabolism. However, CO₂ retention is a consequence of overfeeding, and not overfeeding with carbohydrates.

III. Lipid Complications:

-Overfeeding with lipids may contribute to hepatic steatosis.

-Triggering inflammatory response: The lipid emulsions used in TPN regimens are rich in oxidizable lipids, and the oxidation of infused lipids will trigger an inflammatory response. (Oleic acid, one of the lipids in TPN, is a standard method for producing ARDS in animals), and this might explain why lipid infusions are associated with impaired oxygenation.

IV. Hepatobiliary Complications:

1-Hepatic Steatosis:

-Fat accumulation in the liver (hepatic steatosis) is common in patients receiving long-term TPN and is believed to be the result of chronic overfeeding with carbohydrates and lipids. Although this condition is associated with elevated liver enzymes, it may not be a pathological entity.

2-Cholestasis:

-The absence of lipids in the proximal small bowel prevents cholecystokinin-mediated contraction of the gallbladder. This results in bile stasis and the accumulation of sludge in the gallbladder and can lead to acalculous cholecystitis.

V. Bowel Sepsis:

-The absence of nutritional bulk in the GI tract leads to atrophic changes in the bowel mucosa and impairs bowel-associated immunity, and these changes can lead to the systemic spread of enteric pathogens.

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 Multiple Sclerosis

-Multiple sclerosis (MS) is the most common demyelinating neurological disease.

-The myelin surrounding an axon may develop normally and be lost later, but leaving the axon preserved. Alternatively, there may be some defect in the original formation of myelin as a result of an error in metabolism.

-Multiple sclerosis is thought to be autoimmune in nature. Susceptibility to MS may be genetically determined. Viral and immune factors are possibly involved.

-It is characterized by a combination of inflammation, demyelination, and axonal damage in the CNS. Disruption of the blood-brain barrier is an early event. Plaques of demyelination are scattered throughout the nervous system, usually in the optic nerve, brainstem, and spinal cord. The peripheral nerves are not involved.

Preoperative Findings:

1. The commonest presenting symptoms, in order of frequency, are limb weakness, visual disturbances, paresthesia, and incoordination. Legs are more commonly involved before the arms, with signs of spasticity and hyperreflexia. Urinary symptoms may occur.

2. Progression, with remissions and relapses, is very variable. Infection, trauma, and stress may be associated with relapses. A small increase in body temperature can cause a definite deterioration in neural function. The third trimester of pregnancy is associated with a 70% decrease in relapse rate, but this is followed by an increase of about 70% in the first 3 months postpartum. This may impair the ability of a mother to care for her baby.

3. Pain may be a prominent feature, occurring in 45% of patients.

4. Mild dementia and dysarthria may appear as the disease progresses.

5. In advanced disease, and sometimes earlier during acute relapses, respiratory complications may occur secondary to a variety of causes; they were, in decreasing order of importance, respiratory muscle weakness, bulbar weakness, and central control of breathing.

6. MRI now plays an important part in the diagnosis, and abnormalities in the white matter can be seen in 99% of cases. Gadolinium enhancement seems to reflect areas of inflammation where the blood-brain barrier has broken down.

7. Patients are treated with; baclofen, gabapentin, or beta interferon.

Anesthetic Problems:

1. Both experimentally and clinically, an increase in body temperature has been shown to cause a deterioration in nerve conduction and neurological signs.

2. Spinal anesthesia is associated with an increased incidence of neurological complications.

3. Epidural anesthesia in pregnant women with MS showed that there was no difference between those who had been given an epidural and those who had not. Temporary neurological deficits have, however, been reported. It was postulated that neurotoxicity might have resulted from the diffusion of the local anesthetic into the dural space. However, it has been suggested that concentrations of bupivacaine of not greater than 0.25% should be used since postpartum relapse has been reported with those above this.

4. Local anesthesia did not significantly increase the relapse rate. However, early disruption of the blood-brain barrier in MS means that local anesthetics can cross more readily, and toxicity is more likely to occur.

5. Neuromuscular blockers. Resistance to atracurium, in association with an abnormally high concentration of skeletal muscle acetylcholine receptors, has been reported in a patient with MS and spastic paraparesis.

6. There is an increased incidence of epilepsy in MS patients.

Anesthetic Management:

1. Elective surgery should not be undertaken in the presence of fever.

2. Spinal anesthesia should probably be avoided. If a regional block is required, epidural anesthesia is preferable.

3. The maximum dose of local anesthetic should be reduced below that normally recommended. Techniques that require large doses should be avoided.

4. It was suggested that IV gamma globulin immediately after delivery protects patients from relapse in the first 6 months postpartum.

5. Patients may require treatment for pain and spasticity.

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Post-Tonsillectomy Bleeding

Incidence and Initial Management:

-The incidence of post-tonsillectomy bleeding ranges from 2% to 4%. It is more common in teenagers and young adults than in small children. The vast majority of postoperative bleeding occurs between days 5 and 10 when the eschar separates from the tonsil beds. In rare cases, bleeding may occur in the immediate postoperative period.

-Initial management is tailored to the degree of bleeding. The clot in the tonsillar bed should be suctioned, as spontaneous hemostasis is rare with the clot in place.

-Minimal bleeding may resolve with an ice water gargle or hydrogen peroxide gargle, and older children may tolerate the application of a cautery stick with silver nitrate while awake.

-Administration of antifibrinolytics as tranexamic acid.

-Significant bleeding in a young child, however, typically involves a return to the operating room for a thorough examination of the pharynx and electrocautery hemostasis.

Preoperative Assessment and Optimization:

1-Airway Assessment:

-Although it may be difficult to assess the airway in-depth in an agitated child, observation of the external anatomy and information about airway management from the prior anesthetic should provide sufficient information.

-Even though airway management was uncomplicated previously, it may be more difficult at this time because of postoperative edema and blood obscuring visualization of the larynx.

2-Intravascular Volume Status:

-It is possible to underestimate the degree of blood loss, since much of it may have been swallowed. Heart rate, blood pressure, and, if possible, orthostatic testing will provide information regarding volume status and guide volume resuscitation.

-Assessing for the presence of tears, moist mucus membranes, skin turgor, and urine output will be helpful as well.

-Adequate IV access, with a large-bore intravenous catheter, should be obtained, if not already present.

-Intraosseous access should be entertained in the hypovolemic, hypotensive patient if IV access cannot be obtained in a timely fashion.

-Volume resuscitation should be initiated with non-glucose-containing isotonic fluids. If the patient is hypotensive, 20 mL/kg boluses of isotonic fluid should be administered until the blood pressure normalizes.

-Transfuse red blood cells if hemodynamically unstable and hematocrit is low.

-Once the bleeding has been controlled and the patient is normovolemic, maintenance fluids should be continued.

3-Laboratory Tests:

-Hematocrit, platelet count, electrolytes, and coagulation studies.

-A specimen should also be sent for serotyping and cross match, as transfusion is a very real possibility.

-Surgery should not be delayed waiting for test results, since bleeding will continue without surgical intervention

Intraoperative Management:

-Management of the airway is of major concern, particularly the ability to visualize the larynx in the presence of ongoing bleeding.

-In preparation for induction, the following should be prepared: multiple laryngoscope blades, a styletted cuffed ETT, and large bore suction.

-The otolaryngologist should be present and tracheostomy equipment immediately available should a surgical airway become necessary.

-The patient is considered to have a full stomach, even if they have not recently eaten, because of swallowed blood.

-A rapid sequence induction is usually performed. However, in the situation where there is significant concern about the airway, a smooth mask inhalation induction with cricoid pressure can be performed with the patient in the right lateral decubitus position with the head down (tonsillectomy position) with suction immediately available. The tonsillectomy position minimizes aspiration risk by promoting the pooling of blood in the oropharynx.

-The choice of IV induction agent will depend on the volume status. Ketamine or etomidate may be used if there is ongoing concern about volume status and hemodynamic stability. Alternatively, propofol may be used but in a decreased dose.

-Muscle relaxation can be achieved with either succinylcholine or rocuronium. However, the duration of action of rocuronium at the dose recommended for rapid sequence induction (1.2 mg/kg) will likely exceed the length of the procedure.

-Volume status should be continually assessed in the face of ongoing bleeding and managed appropriately with isotonic fluids.

-The hematocrit, degree of hemodynamic stability, and status of hemostasis will dictate the need for a blood transfusion.

-Replacement of coagulation factors is rarely necessary. However, if a previously undiagnosed coagulopathy is discovered, the appropriate therapy should be initiated and a hematology consult obtained.

Postoperative Management:

-Patients should be placed in the lateral decubitus position with the head down with supplemental oxygen for transport to the PACU.

-Analgesic and antiemetic medications should be ordered.

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