- Anesthesia Morbidity and Mortality

Failed Epidural Block

By Author August 18, 2019

Failed Epidural Block

Introduction:

➧ Failure of epidural anesthesia and analgesia occurs in up to 30% of clinical practices.

➧ Some technical factors can help to increase the primary and secondary success rates.

A) Technical factors influencing block success:

1-Patient Position:

➧ Patient positioning potentially affects needle placement by changing the relationship between osseous and soft tissues.

a) Sitting Position

➧ Results in shorter insertion times and higher accuracy at the first attempt than in the lateral position.

➧ Causes more vagal reflexes than lateral position.

➧ This leads to epidural venous plexus distension, which may theoretically increase the risk of vascular puncture, especially in parturients.

b) Lateral Position

➧ Increases the distance from the skin to the epidural space.

➧ Results in more technical difficulties compared with the sitting position.

2-Puncture Site:

➧ Inaccurate dermatomal block-level or anatomical landmarks of neuraxial puncture are not suitable for the type of surgery.

3-Approach:

a) Midline Approach

➧ Results in a higher incidence of paresthesia than the paramedian approach.

➧ Results in a bloody puncture in non-pregnant adults than paramedian approach.

➧ The ligamentum flavum is not continuous in all patients, and the presence of midline gaps may make the loss of resistance (LoR) to needle advancement and injection of air/saline less perceptible when the midline approach is used.

b) Paramedian Approach

➧ Results in faster catheter insertion times, and less dependent upon spine flexion.

➧ Paramedian catheters cause less epidural tenting, and pass cephalad more reliably than midline catheters.

4-Identification of the Epidural Space:

➧ Correct placement obviously requires correct identification of the epidural space. The LoR using saline has become the most widely used method, while LoR to air and the hanging drop technique is less widely used with no difference in the success rate or adverse events, other than a 1.5% reduction in post-dural puncture headache [1] when using saline.

➧ In obstetric epidurals, using saline for LoR results in fewer attempts than using air, but with comparable final success rates.

➧ The use of the ‘preferred technique’ (i.e. the technique used by anesthetists 70% of the time) results in significantly fewer attempts, a lower incidence of paresthesia, and fewer dural punctures, irrespective of whether saline or air is used for LoR.

➧ The hanging drop technique depends on negative pressure within the epidural space and is useful only in the sitting position.

➧ Identification of the epidural space was reported at 2 mm deeper for the hanging drop when compared with LoR, possibly indicating an increased risk of dural puncture.

➧ Ultrasound pre-assessment of lumbar epidural space depth has been shown to correlate well with actual puncture depth in obese parturients.

➧ The use of ultrasound led to less bony contact, a shorter time to block success, and decreased supplemental opioid requirements.

5-Epidural Catheter Location:

➧ Epidural catheters may primarily be placed incorrectly, or become dislodged during operation.

➧ Primary misplacement of epidural catheters in the paravertebral space, in the pleural cavity, or intravascularly.

➧ Transforaminal migration of the catheter tip and asymmetric spread during epidural analgesia.

➧ During normal patient movement, epidural catheters may be displaced by centimeters.

➧ Changes in epidural pressure and cerebrospinal fluid (CSF) oscillations can contribute to the displacement of epidural catheters.

➧ Midline fat pedicles may form a barrier to the spread of local anesthetics (LA).

6-Catheter Insertion and Fixation:

➧ The catheter should be inserted at least 4 cm into the epidural space.

➧ Suturing of the epidural catheter is associated with less migration, but at the cost of increased inflammation at the puncture site.

➧ Tunneling the epidural catheter for 5 cm is associated with less movement of the catheter and decreases catheter migration but it will not maintain the original position.

➧ Tunneling caudal epidural catheter in children reduces the risk of bacterial colonization to levels comparable to untunneled lumbar catheters because tunneling places the catheter entry point above the diaper in babies and toddlers.

➧ For lumbar and epidural catheters, the advantages of tunneling are less obvious and the need to prevent dislodgement must be weighed against the increased incidence of erythema at the puncture site, potentially linked to increased risk of bacterial colonization.

➧ Catheter fixation devices are available which may significantly reduce migration percentage and reduce rates of analgesic failure.

7-Test Dose:

➧ A test dose is given with two main objectives of detecting intrathecal or intravascular catheter placement.

➧ A test dose of lidocaine (to detect intrathecal placement) and epinephrine (to detect intravascular placement) is recommended in patients without contraindications to epinephrine.

➧ Specific regimens to detect intravascular catheter position:

-Fixed epinephrine test dose for non-pregnant adult patients.

-Fentanyl test dose for parturients.

-Weight-adjusted epinephrine test dose for children.

➧ Patients sensitive to intravascular epinephrine (parturients, patients with cardiac or vascular disease) may experience undesirable side effects if the test is positive. However, this risk is outweighed by the systemic toxic effects of LA if the intravascular placement was not detected.

8-Equipments:

➧ The orifice of the catheter can lie laterally or anteriorly in the epidural space putting the LA more to one side and producing a unilateral block. In general, multi-orifice catheters are considered better than single-orifice catheters.

➧ Manufacturing errors, such as faulty markings on the epidural catheter, can lead to a wrong depth of placement.

➧ Debris in the catheter or disconnection can cause epidural failure.

➧ Obstruction of the epidural infusion system by an airlock, as little as 0.3–0.7 ml of air, in the bacterial filter.

➧ The knotting of the catheter internally or externally can cause obstruction.

➧ Removal of a presumed knotted catheter can be attempted after sensation has returned to monitor neurological symptoms during catheter removal. When radicular symptoms or pain occur during the removal of a catheter, this should be immediately stopped. It has been found that removal is easiest if the patient is in the same position as at insertion. Surgical removal of a broken catheter is not compulsory if the patient remains asymptomatic.

References:

1. Shaat AM, Abdalgaleil MM. Is theophylline more effective than sumatriptan in the treatment of post-dural puncture headache? A randomized clinical trial. Egyptian Journal of Anaesthesia 2021; 37(1): 310-316. https://doi.org/10.1080/11101849.2021.1949195.

Anesthetic Precautions for Bloody and Lengthy Surgery

By Author August 16, 2019

Anesthetic Precautions for Bloody and Lengthy Surgery

A) Precautions for Bloody Surgery

1-Decrease blood loss by:

➧ The surgical site elevation is 10-15°

➧ Use of tourniquet

➧ Local infiltration of epinephrine

➧ Use of topical hemostats

➧ Application of hypotensive anesthesia

➧ Controlled mechanical ventilation (decrease venous return → decrease Cardiac output and PaCO₂)

➧ Use antifibrinolytic agents: (Aprotinin, Epsilon Amino Caproic Acid, Tranexamic acid)

➧ Use desmopressin (DDAVP)

➧ Keep patient normothermic

➧ Give IV Calcium (to prevent citrate toxicity and help coagulation)

➧ Restrict diagnostic phlebotomies

➧ Avoid: (Atropine, Ketamine, Pancuronium) (increase: Heart rate, Blood pressure, Endogenous catecholamines)

2-Restore Blood loss rapidly by:

➧ Prepare type-specific, cross-matched blood

➧ Preoperative autologous blood donation

➧ Apply normovolemic hemodilution

➧ Use cell saver devices (Blood Salvage)

➧ Insert wide bore IV cannulae

➧ Use blood substitutes

➧ Use rapid infusion devices

➧ Use blood warmers

B) Precautions for Lengthy Surgery

1-Decrease Hypothermia by:

➧ Monitoring by a temperature probe

➧ Increase ambient room temp. ≥ 24° (in Adults), ≥ 26° (in Pediatrics)

➧ Cotton wrapping of the limbs and head

➧ Use a warming blanket/mattress

➧ Warm IV fluids

➧ Warm irrigating fluids

➧ Warm humidified inspired gases

➧ Use low flow anesthesia

➧ Use blood warmers

2-DVT prophylaxis.

3-Pressure sore prophylaxis (Padding of pressure points).

4-Eye protection (Tap and Pad).

5-Invasive monitoring (CVP, IBP).

6-Avoid N₂O (causes: Bone marrow depression, Megaloblastic anemia, Agranulocytosis, Peripheral neuritis, Immune response depression).

7-Use Isoflurane (More rapid recovery).

8-Insert nasogastric tube (to avoid gastric distension).

9-Use high volume, low-pressure ETT cuff (with frequent monitoring of intracuff pressure or use intracuff saline).

10-Avoid hypovolemia (by: Monitoring, Fluid chart, IV fluids).

Minimally Invasive and Non-invasive Cardiac Output Monitoring

By Author August 14, 2019

Minimally Invasive and Non-invasive Cardiac Output Monitoring

➧ The concept of determining blood flow/time Cardiac Output (CO) by measuring the dilution of a ‘known substance’ in the blood (Fick’s principle) has been applied by pulmonary artery (PA) catheter using the thermodilution technique remains the ‘Gold standard’ approach of CO monitoring. However, it is not without risk.

I. Esophageal Doppler U/S:

Principle:

➧ It measures blood flow velocity in the descending thoracic aorta by using the change in frequency of the U/S beam as it reflects off a moving object (Doppler shift).

➧ If this measurement is combined with an estimate of the cross-sectional area of the aorta (derived value from pt. age, height & weight using nomograms), it allows hemodynamic variables to be calculated [Stroke Volume (SV), CO, Cardiac Index (CI)].

Advantage:

➧ Provides continuous measurements

Limitations:

➧ The following three conditions must be met to guarantee accuracy:

1-The cross-sectional area must be accurate.

2-The US beam must be directed parallel to the flow of blood

3-The beam direction cannot move to any great degree between measurements.

➧ Variations in the above conditions lead to inaccuracies.

Disadvantages:

➧ The main problem with its use as a continuous CO monitor relates to its precision which indicates the reproducibility of a measurement.

➧ It is operator dependent and it is very easy for the position of the probe to change between measurements which will reduce the precision.

➧ The need for frequent repositioning is not well tolerated by an awake pt. and is therefore need sedation.

II. Echocardiography: [Trans-Thoracic & Trans-Esophageal (TEE)]

Principle:

➧ This technique can be used to calculate SV which can then be multiplied by HR to give the CO.

➧ For the assessment of SV; 2 steps are necessary:

1- Calculation of flow velocity from the area under the Doppler velocity wave. This represents the distance RBCs are projected forward in one cardiac cycle.

2- Determination of area through which the flow is pushed forward (calculated from the diameter assuming a circular shape or determined by direct planimetry). Measurements can be performed at the level of [PA, Mitral Valve (MV), or Aortic Valve (AV)].

Advantage:

➧ Good correlation with thermodilution CO measurements providing that the MV is competent.

Limitations:

➧ It is very difficult to measure the diameter of PA.

➧ Measurement at MV is even more difficult because the shape & size of the valve changes during the cardiac cycle

➧ The AV is the third option for Doppler assessment which can be performed using transgastric or deep transgastric views. In the absence of aortic stenosis, this method is the most accurate for CO measurements.

Disadvantages:

➧ TEE cannot be tolerated by an awake patient as a continuous CO monitor.

➧ Esophageal injury by the probe.

➧ Mediastinitis.

III. Thoracic Electrical Bioimpedance:

Principle:

➧ Changes in thoracic volume cause changes in thoracic resistance (bioimpedance) to “low amplitude, high frequency” currents. If thoracic changes in bioimpedance are measured following ventricular depolarization, SV can be continuously determined.

➧ Increasing fluid in the chest results in less electrical bioimpedance.

➧ This noninvasive technique requires 6-electrodes to inject microcurrents & to sense bioimpedance on both sides of the chest.

➧ Mathematical assumptions and correlations are then made to calculate CO from changes in bioimpedance.

Advantage:

➧ Simple, quick, non-invasive with minimal pt. risk.

Limitations:

➧ The accuracy is questionable in several groups of pt., e.g.; those with AV disease, previous heart surgery, or acute changes in thoracic sympathetic nervous function (e.g., those undergoing spinal a.).

Disadvantages:

➧ Electrode susceptibility to electrical interference.

➧ Electrode placement is an important source of error.

➧ Measurements influenced by intrathoracic fluid shifts and changes in Hct.

IV. Thoracic Bioreactance:

Principle:

➧ Because of the limitations of bioimpedance devices, newer methods of processing the impedance signal have been developed. The most promising technology to reach the marketplace is the NICOM device (Cheetah Medical, Portland, OR), which measures the bioreactance or the phase shift in voltage across the thorax.

➧ The human thorax can be described as an electric circuit with a Resistor (R) and a capacitor (C), which together create the thoracic impedance (Zo).

➧ The values of R and C determine the two components of impedance, which are:

(1) Amplitude (a), the magnitude of the impedance (measured in ohms)

(2) Phase (phi), the direction of the impedance (measured in degrees)

➧ The pulsatile ejection of blood from the heart modifies the value of R and the value of C, leading to instantaneous changes in the amplitude and the phase of Zo. Phase shifts can occur only because of pulsatile flow.

➧ The majority of thoracic pulsatile flow comes from the aorta. Therefore, the NICOM signal is correlated almost totally with the aortic flow.

➧ Furthermore, because the underlying level of thoracic fluid is relatively static, neither the underlying levels of thoracic fluids nor their changes induce any phase shifts and do not contribute to the NICOM signal.

➧ The NICOM monitor contains a highly sensitive phase detector that continuously captures thoracic phase shifts, which together result in the NICOM signal.

➧ NICOM is totally non-invasive. This system consists of a high-frequency (75 kHz) Sine wave generator and 4-dual electrode “stickers” that are used to establish electric contact with the body.

➧ Each sticker has two electrodes, one electrode is used by the high-frequency current generator to inject the high-frequency sine wave into the body, whereas the other electrode is used by the voltage input amplifier.

➧ Two stickers are placed on the right side of the body, and two stickers are placed on the left side of the body. The stickers on a given side of the body are paired, so the currents are passed between the outer electrodes of the pair, and voltages are recorded from between the inner electrodes.

➧ Thus, a non-invasive CO measurement signal is determined separately from each side of the body, and the final noninvasive CO measurement signal is obtained by averaging these two signals.

➧ The system’s signal processing unit determines the relative phase shift (∆ɸ) between the input and output signals. The peak rate of change of ɸ (dɸ/dtmax) is proportional to the peak aortic flow during each beat.

➧ The SV is calculated from the following formula: SV = C × VET × dɸ/dtmax, where C is a constant of proportionality and Ventricular Ejection Time (VET) is determined from the NICOM and electrocardiographic signals.

Advantage:

➧ Totally non-invasive.

➧ Unlike bioimpedance, bioreactance-based CO measurements do not use the static impedance (Zo) and do not depend on the distance between the electrodes for the calculations of SV, both factors that reduce the reliability of the result.

➧ NICOM averages the signal over 1 minute, therefore allowing “accurate” determination of CO in patients with atrial and ventricular arrhythmias.

➧ NICOM assessment of the CO can be performed in ventilated and non-ventilated patients alike.

➧ It is very easy to set up with a high degree of acceptability by nursing staff.

➧ NICOM assessment of the CO can be performed in the emergency room, intensive care unit, and operating room.

Limitations & Disadvantages:

➧ Electrocautery interferes with the NICOM signal. However, as long as the device receives a single for at least 20 sec. within a minute, the CO can be determined. When electrocautery is on for more than 40 sec. in a given minute, the CO for that minute is not displayed.

V. Lithium Dilution CO (LiDCO):

Principle:

➧ Depends on the “indicator dilution technique” which is minimally invasive, requiring only venous (central or peripheral) & arterial lines.

➧ The indicator is isotonic lithium chloride (LiCl) which is injected as a very small bolus (0.3 mmol) via the venous line. LiCl is not normally present in the plasma & not metabolized, and is excreted almost entirely in the urine.

➧ LiCl sensitive sensor, attached to the peripheral arterial line, detects the concentration of LiCl ions in the arterial blood.

➧ The LiCl indicator dilution “wash-out” curve provides an accurate absolute CO value.

Advantage:

➧ Simple and Minimally invasive,

➧ As accurate as, or more accurate than bolus thermodilution.

➧ Safe and does not elicit any hemodynamic changes that are sometimes seen with injections of cold saline.

Limitations & Disadvantages:

➧ The clinical margin of safety: Although the amount of LiCl injected is 100 lower than the lowest clinical doses of ‘lithium-treated patients’, it is recommended to administer not more than 10-20 boluses of lithium.

➧ Side-effects of multiple injections over a short time need to be investigated.

VI. Pulse Pressure Analysis Techniques: (Pulse Contour Analysis Devices)

Principle:

➧ Utilize the arterial pressure tracing curve to estimate the CO and other dynamic parameters; [SV, Systemic Vascular Resistance (SVR), and Blood Pressure (BP)].

➧ It measures the area of the systolic portion of the arterial pressure trace from end-diastole to the end of ventricular ejection, together with an individual calibration factor to account for individual vascular compliance.

➧ Some devices use thermo- or Li-dilution for calibration for subsequent measurement.

➧ Some devices (“FloTrac”; Edwards Life Sciences) do not require calibration with another measure and rely upon statistical analysis and algorithm.

Advantage:

➧ Offers ‘beat-to-beat’ Continuous, non-invasive CO measurement.

➧ Reliable, accurate, precise, and comparable to PA-thermodilution.

➧ Frequent recalibration or even no-calibration (“FloTrac”) is not required.

Limitations & Disadvantages:

➧ Cost.

Fat Embolism Syndrome (FES)

By Author August 13, 2019

Fat Embolism Syndrome (FES)

➧ Fat embolism can be difficult to diagnose. It most often follows a closed fracture of a long bone but there are many other causes.

Epidemiology:

➧ Incidence of this complication ranges from 0.5-to 11% in different studies. It varies considerably according to the cause. Patients with fractures involving the middle and proximal parts of the femoral shaft are more likely to experience fat embolism. Age also seems to be a factor with young men at the highest risk.

Etiology:

1-Fractures: Closed fractures produce more emboli than open fractures. Long bones, pelvis, and ribs cause more emboli. Sternum and clavicle cause less. Multiple fractures produce more emboli.

2- Orthopedic Procedures: Intramedullary nailing of long bones, Fixation of cemented hip prosthesis.

3-Massive soft tissue injury

4-Severe burns

5-Liposuction

6-Bone marrow biopsy

7-Bone marrow harvesting and transplant

8-Cardio-pulmonary bypass

9-Non-traumatic settings occasionally lead to fat embolism. These include conditions associated with:

-Fatty liver

-Acute pancreatitis

-DM

-Osteomyelitis

-Bone tumor Lysis

-Pathological fractures

-Sickle cell crisis (causing bone infarcts)

-Decompression sickness

-Prolonged corticosteroids therapy

-Cyclosporine A solvent

-Parenteral lipid infusion

Sevitt’s classification:

1-Subclinical (Incomplete) form: Fat emboli present in blood and lungs, no symptoms/signs

2-Non-fulminant (Classic) form: Pulmonary dysfunction, cerebral dysfunction, petechiae

3-Fulminant form: Rare, rapid onset (within hours) of acute cor-pulmonale, respiratory failure, coma, and death.

Principal clinical features (triad) of FES:

1-Respiratory failure (dyspnea and hypoxia)

2-Cerebral dysfunction (confusion)

3-Petechiae

➧ Clinical features usually present between 24-72 h. after trauma (lucid interval). This is especially after fractures, when fat droplets act as emboli, becoming impacted in the pulmonary microvasculature and other microvascular beds, especially in the brain.

➧ Embolism begins rather slowly and attains a maximum in about 48 h.

➧ The initial symptoms are probably caused by mechanical occlusion of multiple blood vessels with fat globules that are too large to pass through the capillaries.

➧ The vascular occlusion in fat embolism is often temporary or incomplete as fat globules do not completely obstruct capillary blood flow because of their fluidity and deformability.

➧ The late presentation is thought to be a result of hydrolysis of the fat to more irritating free fatty acids which then migrate to other organs via the systemic circulation.

➧ It has also been suggested that paradoxical embolism occurs from shunting.

Clinical Presentation:

➧ There is usually a latent period of 24-72 h. between injury and onset.

➧ Symptoms: There is vague pain in the chest and shortness of breath.

➧ Signs: The onset is sudden, with:

-Restlessness

-Fever occurs, often at more than 38.3° C with a disproportionate tachycardia.

-Drowsiness with oliguria is almost pathognomonic.

➧ CNS signs: including a change in the level of consciousness, are common. They are usually non-specific and have the features of diffuse encephalopathy with acute confusion, stupor, coma, rigidity, or convulsions. Cerebral edema contributes to neurological deterioration.

Diagnostic Criteria:

A) Gurd's and Wilson’s Criteria:

-Diagnosis requires at least one sign from the major criteria and at least four signs from the minor criteria. (Table 1)

Table 1: Gurd's and Wilson’s Criteria

B) Schönfeld’s Criteria:

-Diagnosis requires a score of more than 5. (Table 2)

Table 2: Schönfeld’s Criteria

C) The clinical diagnosis is assured if all three of the following criteria are present within 72 h. after traumatic fracture:

1-Unexplained dyspnea, tachypnea, arterial hypoxia with cyanosis, and diffuse alveolar infiltrates on chest X-ray.

2-Unexplained signs of cerebral dysfunction, such as confusion, delirium, or coma.

3-Petechiae over the upper half of the body, conjunctiva, oral mucosa, and retina.

Differential Diagnosis:

➧ Dyspnea, hypoxia, and abnormal CXR: can occur with thrombo-embolism and pneumonia.

➧ Cerebral dysfunction: can occur with hypoxia or meningitis but the rash of meningococcal septicemia is all over and spreads rapidly. It can also occur as a late feature of head injury.

➧ Thrombotic Thrombocytopenic Purpura (TTP).

Investigations:

CBC:

-Hematocrit: is decreased, occurs within 24-48 h., and is due to intra-alveolar hemorrhage.

-Platelets: are decreased.

Serum Lipase: is increased, but this is not pathognomonic as it occurs in any bone trauma.

Serum Calcium: is decreased.

Cytological Examination: urine, blood, and sputum may detect fat globules that are either free or in macrophages. This test has low sensitivity and a negative result does not exclude fat embolism.

Arterial Blood Gases: will show hypoxia, PaO₂ usually less than 60 mmHg, and hypocapnia. Continuous pulse oximeter monitoring may enable hypoxia from fat embolism to be detected in at-risk patients before it is clinically apparent.

ECG: Ischemia, Rt. Ventricular strain, Rt. Axis deviation, RBBB, Arrhythmia.

Chest X-ray: may show evenly distributed, fleck-like pulmonary shadows (Snow Storm appearance), increased pulmonary markings, and dilatation of the right side of the heart.

CT Head: (to rule out intracranial pathology).

CT Chest: (to rule out chest pathology).

Management:

A) Supportive

1-Ensuring good arterial oxygenation: High flow rate of oxygen is given to maintain the arterial oxygen tension in the normal range.

2-Restriction of fluid intake and Diuretics: to minimize fluid accumulation in the lungs so long as circulation is maintained.

3-Maintenance of intravascular volume: is important because shock can exacerbate the lung injury caused by FES. Albumin has been recommended for volume resuscitation in addition to the balanced electrolyte solution, because it not only restores blood volume but also binds fatty acids, and may decrease the extent of lung injury.

4-Mechanical ventilation (APRV) and Positive End-Expiratory Pressure (PEEP): may be required to maintain arterial oxygenation.

B) Pharmacological

1-Corticosteroids: Methylprednisolone (membrane stabilizer, decreases endothelial damage caused by free fatty acids).

2-Low dose heparin: 2500 u / 6 h. (reduce the degree of pulmonary comprise and intravascular coagulation despite the risk of hemorrhage and intravascular lipolysis).

3-Dextran-40: (decreases intravascular thrombosis when ESR is elevated).

4-Ethanol: (decreases lipolysis)

5-Dextrose: (decreases free fatty acid mobilization)

6-DVT prophylaxis

7-Nutrition

C) Surgical:

1-Prompt surgical stabilization of long bone fractures within 24 h. reduces the risk of the syndrome.

2-Use of vacuum or venting during reaming of long bones.

3-Prophylactic IVC filter in at-risk patients.

Prognosis:

➧ The mortality rate from FES is 5-15%. Even severe respiratory failure associated with fat embolism seldom leads to death.

➧ The prognosis is worse in older patients and those with more severe injury but is not affected by gender.

➧ Criteria of bad prognosis: Sevitt’s class, Serum lipase, Lipuria, ARDS.

Prevention:

➧ Early immobilization of fractures seems to be the most effective way of reducing the incidence of this condition.

Peripartum Cardiomyopathy (PPCM)

By Author August 12, 2019

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.