Evaluation of Morbid Obese Patient

Preoperative Anesthetic Evaluation of Morbid Obese Patient

Goals:

1-Obtain data regarding the patient’s medical and surgical history.

2-Optimize current physiologic function.

3-Prepare an appropriate anesthetic plan.

1-Medications:

➧ The obese person must be assessed for the use of weight-reducing substances, herbal supplements, and anorexiant drugs.

➧ Chronic use of noradrenergic and serotonergic therapy can produce hypertension, tachycardia, anxiety, psychosis, and catecholamine depletion.

➧ Catecholamine depletion can lead to profound hypotension during induction and maintenance of anesthesia, which is refractory to indirect-acting vasopressors such as ephedrine.

➧ Phenylephrine hydrochloride (Neo-Synephrine) is usually effective in reversing low blood pressure.

➧ At least two weeks of abstinence from the drugs is recommended for adequate catecholamine levels to be recovered.

2-Laboratory Tests:

➧ Complete blood cell counts: may reveal Hct as high as 65%, which can result from contracted blood volume or polycythemia associated with cardiopulmonary disease.

- Leukocytosis (greater than 11,000) is a strong predictor of risk for acute myocardial infarction independent of tobacco smoking.

➧ Arterial blood gas analysis: that compares samples taken with the patient lying supine and sitting while breathing room provides baseline values and can distinguish simple obesity from Obesity Hypoventilation Syndrome.

➧ Renal function tests and Electrolytes: may reflect abnormal glucose and potassium levels, which are indicators of insulin resistance and potentiation of myocardial irritability.

- Diuretics and certain cardiac medications can worsen electrolyte disturbances.

- Blood urea nitrogen (BUN) and creatinine levels may be elevated in response to dehydration or renal dysfunction.

➧ Liver function tests: are typically elevated in obese patients, it is due to the infiltration of the hepatocytes with triglycerides (fatty liver, liver steatosis).

- The severity of fatty infiltration may alter the pharmacologic effects of many anesthetic drugs, thereby requiring dose reductions.

➧ Coagulation studies are necessary if regional anesthesia is planned or if coagulopathy exists.

- Patients taking anticoagulants for treatment of deep vein thrombosis or atrial fibrillation may exhibit elevated prothrombin and partial thromboplastin times.

- Nonsteroidal anti-inflammatory drugs may prolong bleeding times and affect surgical hemostasis.

➧ Pulmonary function tests: for obese patients undergoing abdominal or thoracic surgery to assist with the anesthetic planning.

➧ Chest radiography: is necessary to determine the presence of cardiomegaly, pulmonary infiltrates, and evidence of COPD.

3-Cardiac Assessment:

➧ History of prior MI, presence of HTN, angina, or PVD is crucial.

➧ Drug history gives clues about the patient's coexistent diseases.

➧ When possible cardiac medications should be continued up to the morning of surgery.

➧ Exercise tolerance: elicit valuable information about the myocardial function in morbidly obese patients.

- Limitations in exercise tolerance, history of orthopnea, and paroxysmal nocturnal dyspnea may indicate left ventricular dysfunction.

➧ ECG: is essential for the determination of resting rate, rhythm, and ventricular hypertrophy or strain. 

➧ Echocardiography: is useful for determining whether akinesis or wall motion abnormalities are present in the obese myocardium.

➧ Chest radiography: to identify pulmonary congestion, elevated diaphragm, and a tortuous aorta.

- The results of the radiographic study serve to guide preoperative pharmacologic and medical management (diuretics, beta-1 agonists, antibiotics).

4-Respiratory Evaluation:

➧ History of orthopnea, wheezing, sputum production, or smoking history.

➧ Recent upper respiratory infections, snoring, or sleep disturbances may indicate obstructive processes.

➧ Careful preoperative evaluation of the patient’s respiratory function identifies potential problems.

➧ A patient who becomes dyspneic and desaturates when recumbent experiences the same symptoms during induction of anesthesia in the supine position.

5-Airway Assessment:

➧ Most anesthetists use the evaluation of multiple patient physical characteristics to identify potential airway problems indicative of the unanticipated difficult airway.

➧ Patient physical characteristics that identify potential airway problems:

- Mallampati classification

- Interincisor distance

- Thyromental distance

- Head and neck extension

- Body weight and BMI

- History of difficult airway

- Length of upper incisors

- Visibility of the uvula

- Shape of the palate

- Compliance with the mandibular space and length

- Short, thick neck

- Pendulous breasts

- Hypertrophied tonsils and adenoids

- Beard

- Marginal room air pulse oximetry saturations

- Abnormal arterial blood gases

- Reduced tempormandibular and antlantooccipital joint movement

- Limited mouth opening, presence of neck or arm pain, or inability to place the head and neck into a sniffing position may indicate the need for awake fiberoptic intubation.

- Increasing neck circumference and Mallampati classification >3 have been identified as the two most important factors for morbidly obese patients.

6-Vascular Access:

➧ Venipuncture can be challenging in obese patients with excessive fat that obscures blood vessels from both visualization and palpation.

➧ Hemorrhage, hypothermia, and trauma also reduce the likelihood of accessing vessels.

➧ Ultrasound-guided central venous catheter placement may improve access and avoid iatrogenic pneumothorax.

7-Patient Education:

➧ Explanations of anticipated events during preoperative preparation: multiple venipunctures, central and arterial line insertions, awake intubation, postoperative ventilation, if needed, pain management, and protection of the patient’s privacy will relieve anxiety.

Read more ☛ Anesthetic Management of Morbid Obese Patient

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Anesthetic Management of Morbid Obese Patient

Anesthetic Management of Morbid Obese Patient

Preoperative:

A) Evaluation:

Read more ☛ Preoperative Anesthetic Evaluation

B) Preparation:

1-Equipments:

➧ New model operating room tables can accommodate up to 270 kg (600 pounds) of weight.

➧ Older model operating room tables could accommodate up to 135-160 kg (300 - 350 pounds) of weight.

➧ In cases of extreme morbid obesity, big-boy hydraulic beds are obtained and used in the operating room.

➧ Extra-large cuffs can be used on the upper/lower extremity. 

➧ Bed warming devices, fluid warmers, and warm airflow blankets should be employed to prevent hypothermia, which can occur rapidly when large areas of the body surface are exposed.

2-Monitoring:

➧ Selection of ECG leads when possible for detection of myocardial ischemia and pathology (leads II and V5).

➧ Placement of an arterial line for the monitoring hemodynamic status is advocated for all but minor procedures.

➧ Central venous and pulmonary artery catheters should be considered in patients undergoing lengthy operations or those with the serious cardio-pulmonary disease.

3-Aspiration prophylaxis:

➧ Obese patients have great volumes and more gastric fluid than people of normal weight.

➧ Gastro-esophageal reflux and hiatus hernia are more prevalent in the obese, predisposing them to esophagitis and pulmonary aspiration.

➧ Conditions that cause delayed gastric emptying, such as DM and traumatic injury, further increase the risk of aspiration.

➧ An obese patient is considered to have a “full stomach,” even if the fasting period is followed.

➧ Pre-induction administration of histamine-2 and dopamine receptor antagonist coupled with oral administration of non-particulate antacids decreases morbidity resulting from pulmonary aspiration and Mendelson’s syndrome.

➧ Head up the position of the patient, with the application of the Sellick's maneuver during rapid-sequence induction, limits the volume of vomitus that enters the trachea if regurgitation occurs.

➧ Nasogastric/Orogastric suctioning before emergence further reduces the amount of fluid available for aspiration.

4-Airway equipment:

➧ Appropriate laryngoscopy blades, handles, endotracheal tubes, masks, oral and nasopharyngeal airways, and stylets should be ready.

➧ Laryngeal mask airways (LMAs), fiberoptic and bronchoscopic devices, Eschman introducers, a jet ventilator (or Venturi apparatus), an emergency tracheotomy, and cricothyrotomy kits must be available if ventilation by mask or endotracheal tube is unsuccessful.

➧ A difficult airway cart with all available equipment should be placed in the operating room.

Intraoperative:

1-Effects of General Anesthesia on Respiration:

➧ General anesthesia depresses respiration in normal subjects so any preexisting pulmonary dysfunction is exaggerated by anesthesia.

➧ General anesthesia reduces FRC by 50% in obese patients, as compared with a 20% reduction in non-obese patients.

➧ FRC can be increased by ventilating with large tidal volumes (15-20 ml/kg), although this has been shown to improve arterial oxygen tension only minimally. Current ventilation recommendations include using tidal volumes of 10-12 ml/kg to avoid barotrauma.

➧ Positive end-expiratory pressure (PEEP) achieves an improvement in both FRC and arterial oxygen tension but at the expense of cardiac output and oxygen delivery.

➧ During laparoscopic surgeries, the respiratory rate should be 12-14 breaths/min.

➧ Prolonged (longer than 2-3 hours) and extensive procedures (involving the abdomen, thorax, and spine) negatively influence respiratory function.

➧ Sub-diaphragmatic packing, cephalad displacement of organs, and surgical retraction cause decreased alveolar ventilation, atelectasis, and pulmonary congestion.

➧ Recumbent/Trendelenburg positioning further reduces diaphragmatic excursion, which is already impaired by the weight of the panniculus, it also causes elevated filling pressures which then increase right ventricular preload.

➧ Myocardial oxygen consumption, cardiac output, pulmonary artery occluding pressures, peak inspiratory pressures, and venous admixtures are increased above upright-sitting values.

➧ In non-obese patients, cardiac output increases in response to supine posturing to maintain hemodynamic stability. By increasing left ventricular output the centrally located circulating volume is propelled forward, thereby minimizing pulmonary congestion and hypoxia.

➧ In morbidly obese patients, positive pressure, ventilation (which impedes venous return), and an inability to increase cardiac output may result in cardiopulmonary decompensation. This is exhibited intraoperatively by hypoxia, rales, ventricular ectopy, congestive heart failure, and hypotension. Bag ventilation by hand may be useful in reducing hypotension resulting from positive pressure.

➧ Adequate ventilator settings inflate the morbidly obese thorax to minimize hypoxia. Pressure or volume-controlled ventilators can be used to maintain adequate oxygenation and normocapnia.

➧ Avoidance of prolonged prone, Trendelenburg or supine positioning also decreases ventilation-perfusion mismatch.

➧ Optimization of oxygenation by using no less than 50% inspired oxygen is recommended.

➧ PEEP can reduce venous admixture and support adequate arterial oxygenation, but PEEP can impair arterial oxygenation in some patients when it is superimposed on large tidal volumes. Recommended PEEP should not exceed 15 cmH₂O.

➧ Intraoperative events, such as hemorrhage or hypotension, further impair ventilatory homeostasis and result in hypoxemia that extends into the postoperative period.

➧ A vertical abdominal incision, compared with a horizontal (transverse incision also prolongs postoperative hypoxia).

➧ Pain causes further reductions in diaphragmatic excursion and vital capacity, leading to atelectasis and ventilation-perfusion mismatch.

➧ 24 h. postoperative admission to a monitored bed is prudent for morbidly obese patients who exhibit higher morbidity and mortality apart from anesthesia and surgery.

2-Choice of Anesthetic Technique:

➧ The selection of the anesthetic technique is dependent on the patient, coexisting history, planned surgical procedure, anesthetist skills and preference, and patient preference.

➧ Anesthetic management of obese patients can include local or monitored anesthesia; general (narcotic, inhalation) anesthesia; regional blocks; or a combination of techniques.

➧ The use of a short-acting water-soluble anesthetic facilitates a smooth anesthetic induction, maintenance, and emergence.

➧ The objective for maintenance of anesthesia in the obese include:

-Strict maintenance of airway

-Optimum oxygenation

-Adequate skeletal muscle relaxation

-Avoidance of the residual effects of muscle relaxants

-Provision of appropriate intraoperative and postoperative tidal volume

-Effective postoperative analgesia

3-Airway Management:

➧ To facilitate airway management, an obese patient should be positioned with the head elevated (reverse Trendelenburg position) on the operating room table.

➧ This position promotes patient comfort, reduces gastric reflux, provides easier mask ventilation, improves respiratory mechanics, and helps maintain functional residual capacity (FRC).

➧ Reduced FRC in obese patients contributes to the rapid desaturation that occurs with induction of general anesthesia, to attenuate the desaturation and maximize oxygen content in the lungs, patients are pre-oxygenated with 100% oxygen for at least 3-5 min.

➧ The patient's head and neck should be carefully moved into the “sniffing position” by using pillows, doughnuts, or foam head supports.

➧ Without proper support and alignment of the oropharynx and trachea, ventilation may be obstructed and visualization of the laryngeal structures may be obscured.

➧ Some anesthetists make an “Awake Look” to visualize the difficulty of the airway. Careful administration of sedative drugs and application of topical anesthesia to the oropharyngeal structures, possibly including transtracheal and superior laryngeal nerve blocks. Nasal oxygen is used as a supplement during awake laryngoscopy.

➧ If the epiglottic and laryngeal anatomy is easily visible, successful asleep intubation can be done, if not, an intubating LMA or awake fiberoptic intubation should be used.

➧ The endotracheal tube must be safely secured to prevent movement during positioning and surgery.

➧ The anesthetist and another skilled anesthesia provider must also be in attendance during induction of anesthesia because muscle hypotonia in the floor of the mouth, followed by the rapid occurrence of soft tissue obstruction and hypoxia, requires one person to support the mask and airway while another person bag ventilates the patient.

➧ In the case of inability to Intubate/ventilate (CICV), the American Society of Anesthesiologists (ASA) difficult airway algorithm should be followed.

4-Volume Replacement:

➧ In obese patients, the estimated blood volume is actually diminished.

➧ Fat, which contains only 8-10% water, contributes less fluid to total body water than equivalent amounts of muscle.

➧ The percentage of total body water is 60-65% in non-obese adults while in morbid obese it is reduced to 40%; therefore calculation of estimated blood volume should be 45-55 ml/kg of actual body weight rather than 70 ml/kg in non-obese adults.

➧ Accurate volume replacement and avoidance of rapid rehydration lessen cardiopulmonary compromise.

➧ Fluid management is guided by blood pressure, heart rate, and urine output measurements. Dilutional coagulopathy, factor VIII inhibition, and decreased platelet aggregation can result from excessive administration.

➧ Volume expanders should not be administered at greater than 20ml/kg of Ideal Body Weight (IBW).

➧ Blood loss replacement of a 3:1 ratio (3 ml of crystalloid to 1 ml of blood loss) is applicable in morbidly obese patients.

➧ Blood products after careful identification should be replaced according to the patient’s laboratory values and hemodynamic or surgical needs.

5-Intraoperative Positioning:

➧ Surgical positioning of morbidly obese patients necessitates extra precautions for the prevention of nerve, integumentary, and cardiorespiratory compromise.

➧ Many peripheral nerves are subjected to possible ischemia or necrosis, the lunar, brachial plexus, radial, personal, and sphenoid nerves are the most vulnerable to injury in an anesthetized patient. In morbidly obese patients the incidence may be increased because of excessive weight on the anatomic structures.

➧ Care is necessary when one is positioning obese extremities in slings, draping them on Mayo stands, or securing them in lithotomy stirrups.

➧ Prolonged hyperextension, external rotation, or abduction can cause postoperative muscle pain, nerve palsies, or paralysis; therefore less flexion or abduction, and rotation of hips, legs, and arms may be necessary.

➧ Frequently repeated inspections of extremities for color and temperature can help diminish the incidence of positioning-related injuries.

➧ Lower back pain can be aggravated by both spinal and general anesthesia because of ligamentous relaxation that results in loss of lumbar curvature. Surgical towels placed under the lumbar spine before induction will enhance lordosis and reduce postoperative discomfort.

6-Integumentary Concerns:

➧ Decubitus, skin infection and wound dehiscence are exceedingly common in morbidly obese patients, therefore ensure all pressure points are padded and in a proper position.

7-Extubation:

➧ The risk of airway obstruction after extubation is increased in obese patients.

➧ A decision to extubate depends on the evaluation of the ease of mask ventilation and tracheal intubation, the length, and type of surgery, and the presence of preexisting medical conditions, including OSA.

➧ Criteria for extubation consist of:

-Awake state, tidal volume, and respiratory rate at preoperative levels

-Ability to sustain head lift or leg lift for at least 5 seconds

-Constant hand grip

-Effective cough

-Adequate vital capacity of at least 15 ml/kg and inspiratory force of at least -25 to -30 cm H₂0.

➧ Patients must be placed with their heads up or in a sitting position.

➧ If doubt exists regarding the ability of the patient to breathe adequately, the endotracheal tube is left in place.

➧ Extubation over an airway exchange catheter or a fiberoptic bronchoscope may be performed.

8-Regional Anesthesia:

➧ Regional anesthesia can be used as the primary anesthetic in selected cases or as an accompaniment to postoperative pain and mobility management.

➧ Difficulties are frequently encountered with morbidly obese patients as anatomical landmarks are not easily visualized or palpable.

➧ Brachial plexus anesthesia can be hampered by adipose tissue in the axillary region due to an inability to position the arm or undetectable pulses.

➧ Redundant roles of adipose tissue, unsatisfactory ventilation, and the inability of the patient to sustain optimal positioning make neuraxial anesthesia more challenging.

➧ For subarachnoid or epidural anesthesia it is recommended that the patient is sitting upright so that landmarks such as C7 or L3-L4 can be more easily identified and longer needles should be used.

➧ Generous infiltration with local anesthetic will provide greater patient comfort during needle insertion due to the repeated insertions and repositioning.

➧ Another consideration regarding subarachnoid or epidural anesthesia in morbid obese pregnant or surgical patients is the lack of predictability of the spread of local anesthetic. Undesirable cephalad spread of local anesthetic can be obviated by reducing the volume and increasing the patient’s upright sitting time.

Postoperative:

1-Pain Management:

➧ Postoperative pain management is facilitated by the use of oral analgesics, non-steroidal anti-inflammatory drugs, narcotics, patient-controlled analgesia, local infiltration of the surgical site, and epidural anesthesia

➧ Obese patients are more sensitive to the respiratory depressant effects of opioid analgesics; therefore caution and close monitoring are warranted. Supplemental oxygen and pulse oximetry monitoring are mandated.

2-Postoperative Complications:

➧ Morbidity and mortality rates are higher in obese patients than in non-obese patients.

➧ Ventilation abnormalities are exacerbated in obese patients with OSA and OHS and may last for several days.

➧ The maximum decrease in partial pressure of arterial oxygen occurs 2-3 days postoperatively.

➧ The risk of thromboembolism wound infections and atelectasis is amplified in patients with increased BMI.

➧ Thromboembolism is facilitated by immobility (Venous stasis, increased blood viscosity (polycythemia, hypovolemia) increased abdominal pressure, abnormalities in serum procoagulants, and anticoagulants.

➧ Antiembolic stockings and correctly fitting pneumatic compression boots can lessen the occurrence of deep vein thrombosis in the early postoperative period.

➧ Early ambulation and maintenance of vascular volume further reduce the likelihood of clots formation.

➧ Wound infections and pulmonary embolism are 50% higher in obese patients than in non-obese patients.

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Peripartum Cardiomyopathy (PPCM)

Anesthetic Management of Peripartum Cardiomyopathy (PPCM)

➧ It is a form of heart failure affecting females in their last months of pregnancy or early puerperium.

➧ The role of the anesthesiologist is important in the peri-operative and ICU.

Diagnostic Criteria for PPCM:

➧ Development of heart failure within the last month of pregnancy or 6 months postpartum.

➧ Absence of any identifiable cause for heart failure.

➧ Absence of any heart disease before the last month of pregnancy.

➧ Echo- Criteria of LV dysfunction:

-Ejection fraction < 45%.

-Left ventricular fractional shortening < 30%.

-Left ventricular end-diastolic dimension > 2.7 cm/m² BSA.

Risk factors:

-Black race, Family history.

-Advanced maternal age.

-Multiparity, Multiple gestations.

-Obesity, Malnutrition.

-Gestational HTN, Pre-eclampsia, C.S.

-Poor antenatal care, Breastfeeding.

-Alcohol, Cocaine, and Tobacco abuse.

Incidence:

-1 in 4,000 live births.

-This wide variation may be explained by the influence of genetic and environmental factors, as well as different reporting patterns and diagnostic criteria used.

Etiology:

1) Myocarditis

-It is not known whether it is an association or a cause.

-Only diagnosed by histological examination of endometrial biopsy.

-Also, the vasopressor therapy in PPCM may lead to Histological changes resembling myocarditis.

2) Viral Infection

-During pregnancy, there is a degree of depressed immunity that may lead to viral infection. Viral infection has been implicated as a cause of myocarditis that would lead to cardiomyopathy.

-On the other hand, it has been argued that viral cardiomyopathy should not be included as a cause of PPCM. But rather a separate entity.

3) Autoimmune Theory

-Studies hypothesized, that fetal cells may escape to the systemic circulation triggering an immune response.

-Higher rates of PPCM with twin pregnancies and its familial predisposition support this theory.

4) Inflammatory Cytokines

-In PPCM patients, higher concentrations of inflammatory cytokines like TNF α, CRP, and IL-6 were found. CRP levels correlated inversely with left ventricular ejection fraction (LVEF).

5) Selenium Deficiency

-Significantly low selenium concentrations in PPCM patients were found, still, this might be a mere incidental association rather than a cause.

6) Exaggerated Hemodynamic Response

-In pregnancy, there are physiologic changes in the CVS. It has been postulated that PPCM may be an exacerbation of this normal phenomenon.

7) Prolonged Tocolytic Therapy

-Usually, tocolysis causes tachycardia and vasodilation, so it may actually unmask existing heart disease rather than play an etiologic role.

Diagnosis:

-The symptoms & signs are the same as heart failure.

-You have to exclude other causes of heart failure as valvular and IHD.

Symptoms:

-Dyspnea on exertion, cough, orthopnea, and paroxysmal nocturnal dyspnea, resembling left-sided heart failure.

-Non-specific symptoms include palpitations, fatigue, malaise, and abdominal pain.

-Embolic manifestations may be present, as mural cardiac thrombi commonly occur. The patient may complain of chest pain, hemoptysis, and hemiplegia, rarely myocardial infarction may be the presentation due to coronary embolism.

Signs:

-Blood pressure may be normal/elevated/low.

-Tachycardia, Gallop rhythm.

-Engorged neck veins, Pedal edema

-Clinically, the heart may be normal or there may be mitral and/or tricuspid regurgitation with pulmonary crepitations.

Investigations:

➧ ECG: No specific findings.

➧ Chest x-ray: May show: Cardiomegaly, Pulmonary venous congestion.

➧ Echocardiography: It is the most important diagnostic tool, and assesses the severity and the prognosis of PPCM.

Echo findings are:

-Decreased LVEF and LVFS, Increased LVEDD.

-Dilatation of all cardiac chambers with subsequent functional mitral, tricuspid, pulmonary and aortic regurgitation.

➧ Dobutamine stress Echo: is a better prognostic tool than the ordinary Echo.

➧ TEE and Cardiac MRI: are better tools for detecting intramural thrombi than the ordinary Echo.

Complications:

1-Thromboembolism

-Thrombi often form in patients with LVEF < 35% and are associated with a mortality rate of 50%.

2-Arrhythmias

-All kinds of arrhythmias have been reported up to VT and heart arrest.

3-Organ failure

-Acute liver failure and hepatic coma due to passive liver congestion secondary to cardiac failure. Also, multiorgan failure may occur.

4-Obstetric & Perinatal complications

-There is an increased incidence of Abortion, Premature deliveries, IUGR, and Intrauterine fetal deaths.

Management:

A) Non-pharmacological measures:

-As with any heart failure, salt and water restriction (2-4 g/d., 2 L/d.).

-Once the severe symptoms are improved, modest exercise should be encouraged.

B) Pharmacological measures

-As with any heart failure: (Digoxin, Diuretics, VD, and Anticoagulation) are the mainstay.

-But we have to consider the safety of these drugs in pregnancy and lactation:

1-Digoxin

-It is a class C drug but presumed safe in low doses.

-In a pregnant female, the serum level should be monitored.

-Some studies claimed that digoxin for 6 m. decreases the risk of recurrence of PPCM.

2-Diuretics

-They are safe during pregnancy and lactation.

-Aim to reduce preload.

-Usually, loop diuretics are used and thiazides are used in milder cases. Spironolactone is very beneficial in heart failure but is better avoided during pregnancy.

-Should be used with caution not to induce dehydration and uterine hypoperfusion. Also, metabolic alkalosis may develop.

3-Vasodilators

-They reduce the preload and afterload in heart failure, and so increase the CO.

-Hydralazine and Nitrates are the VD of choice during pregnancy.

-ACEI and ARB are the mainstays in heart failure but they are class D, and contraindicated in pregnancy due to teratogenicity. So, they are considered after labor, but breastfeeding has to be discontinued.

4-Calcium Channel Modulators

-Calcium channel blocker: Although has –inotropic, but has been shown to improve the survival in cardiomyopathy patients. it also reduces the level of inflammatory cytokines so they would play an important in PPCM.

-Levosimendan: is especially valuable and used with success in PPCM. but again, breastfeeding should be avoided during its use.

5-Beta Blockers

-Like CCB, BB now has an important role in heart failure and they are not contraindicated in pregnancy, though associated with low birth weight.

-Both BB and ACEI have an additional role in immunosuppression and prevent remodeling and reduce ventricular dimensions.

6-Antiarrhythmic agents

-No antiarrhythmic agent is completely safe in pregnancy.

-Quinidine and Procainamide have a high safety profile, but treatment should always start in a hospital because of the high incidence of torsades de pointes.

-Amiodarone may cause: Hypothyroidism, Growth retardation, and Perinatal death, So it should be reserved for life-threatening arrhythmias only.

7-Anticoagulation therapy

-Anticoagulation therapy targets patients with LVEF < 35%, bedridden, Atrial fibrillation, Mural thrombi, Obese, or with a history of thromboembolism.

-The therapy may persist for as long as 6 w. in the Puerperium.

-Heparin is used in the antepartum and Heparin or Warfarin is used in the postpartum period as warfarin is contraindicated in the antepartum period due to its teratogenicity.

Obstetric management:

-Induction of delivery should be considered if pt. condition deteriorates despite maximal medical management.

-If the pt. is compensated, normal vaginal delivery is preferred.

-If the patient is severely decompensated or there are obstetric indications, C.S. should be done.

-In both cases, the pt. should be admitted to ICU for early detection of complications.

Anesthetic management:

A) Anesthesia for Vaginal Delivery:

-Controlled epidural a. under invasive monitoring is a safe and effective method.

-Sympathectomy induced by epidural leads to afterload and preload reduction that improves myocardial function in PPCM patients.

B) Anesthesia for Cesarean Section:

Both General anesthesia (GA) and Regional a. (RA) have been used.

1-Regional Anesthesia

-Single-shot spinal a. is not preferred, because of its rapid hemodynamic changes and hypotension.

-Epidural a. is used because of its better hemodynamic stability.

-Continuous spinal a., with its lower failure rates, faster onset, good muscle relaxation, less drug requirement, postoperative analgesia facilities, and better maintenance of hemodynamics has also been successfully applied.

-In severely compromised pt.: Local infiltration with Bilateral ilioinguinal blocks has been used.

2-General Anesthesia

-GA may be needed in emergency situations or when RA is contraindicated, particularly in the anticoagulated patient.

-Advantages: Airway control and ventilation, and it facilitates the use of TEE.

-Disadvantage: It can cause maternal and fetal cardiorespiratory depression, and the stress of rapid sequence induction on the decompensated heart could be dangerous. There is also an increased risk of LVF and pulmonary edema. GA does not provide thromboprophylaxis like RA.

-opioid-based anesthesia may be advantageous in compromised cardiac conditions, but carries a high risk of fatal respiratory depression.

-Monitoring: In mild cases, noninvasive monitoring can be used. in severely decompensated cases, the use of invasive monitoring is a must. This includes the use of an arterial line and may be a pulmonary artery catheter.

C) Postoperative management:

-All PPCM patients should be managed in an ICU as they are prone to develop LVF and pulmonary edema during this period. Also, to monitor the possible complications.

-Postoperative pain can be managed by RA or parenteral opioid-based techniques.

Prognosis:

➧ Poor prognosis criteria, the worst prognosis is found in patients with:

-Higher age and parity, Multiple gestations.

-Black race.

-Later onset of symptoms (> 2 w.) after delivery.

-Coexisting medical illness.

-Delay of initiation of medical treatment.

-Intracardiac thrombi, Conduction defects, Persistence of ventricular dysfunction > 6 m.

Risk of Recurrence in subsequent pregnancy:

-The highest risk of recurrence remains in patients with persistent cardiac dysfunction and the lowest risk is in those whose cardiac functions have been normalized, as evidenced by the dobutamine stress test.

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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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