By Z. Jose. Lutheran Bible Institute. 2019.

Echocardiography revealed a moderate apical muscular ventricular septal defect with left to right shunting; there is mild right ventricular dilatation order paroxetine 30mg free shipping. Cardiac catheterization was performed and hemodynamic data showed a signifi- cant left to right shunt with a Qp: Qs ratio of 2 buy 30 mg paroxetine with visa. The angiogram confirmed the diagnosis of a moderate size apical ventricular septal defect buy cheap paroxetine 20 mg on-line. Ventricular septal defect device closure was performed during the catheterization procedure with no adverse effect and effective elimina- tion of left to right shunting generic paroxetine 30mg otc. Defects in the apical region of the ventricular septum are difficult to close surgically due to their loca- tion. Device closure of muscular ventricular defects is now possible using specially made devices. The proximity of the aortic and atrioventricular valves and the con- duction pathways to the membranous, inlet, or outlet ventricular defects, makes it more difficult to close these defects with a device, although experimental attempts are underway to develop such devices and methodologies, particularly those for perimembrenous ventricular septal defects. On the other hand, muscular defects are remotely situated from any vital structures and thus more amenable to device closure. They present with increased work of breathing or an increasing need for mechanical ventilatory support. The murmur in these premature infants tends to be systolic rather than continuous. Pharmacological agents such as indomethacin and ibuprofen are the first line of management in this age group. In the rare instances where this is not pos- sible, surgical ligation is performed. Definition The ductus arteriosus is a vascular structure connecting the left main pulmonary artery to the upper part of the descending aorta just distal to the left subclavian artery. The ductus arteriosus is an important structure in fetal circulation, allowing the right ventricle to pump blood directly to the descending aorta thus bypassing the pulmonary circulation. In normal newborns, the ductus is mostly closed by the second or third day of life and is fully sealed by 2–3 weeks of life. Khalid (*) Children’s Heart Institute, Mary Washington Hospital, 1101 Sam Perry Blvd. The frequency is much higher in premature infants and infants with congenital rubella syndrome and Trisomy 21. Pathology The ductus arteriosus remains patent in utero due to low oxygen tension in the blood and a high level of circulating prostaglandins. Simultaneously, there is a drop in the prostaglandin level due to metabolism in the infant’s lungs and elimination of the placental source. Closure of the ductus is initiated by smooth muscle contraction a few hours after birth. This is followed by enfolding of the endothelium, subintimal disruption and proliferation. The lumen is thus obliterated and the closed ductus is transformed into a fibrous ligament known as the ligamentum arteriosum. Failure of the ductus arteriosus to close results in maintenance of patency and therefore a channel for blood to shunt from the aorta to the pulmonary circulation (Fig. The patent ductus arteriosus connects the aortic arch to the main pulmonary artery at the take-off of the left pulmonary artery. If the ductus arterio- sus fails to close, there will be shunting of blood from the high pressure aorta to the pulmonary circulation. This increased blood volume then returns to the left atrium, left ventricle, and ascending aorta and can cause volume overload and dilatation of these structures (Fig. With prolonged exposure to high pressure and increased flow, the pul- monary vasculature undergoes progressive morphological changes which can lead to pulmonary vascular obstructive disease. The pulmonary vascular resistance is significantly less than the systemic vascular resistance, Any abnormal communication between the left and right sides of the heart will result in left to right shunting. Blood flow to the lungs versus that to the body (Qp:Qs ratio) in this scenario is 6:2 or 3:1. The resulting pulmonary edema can manifest clinically as tachypnea, poor feeding, failure to thrive, recurrent respira- tory infections, or congestive heart failure. Blood shunting from the aorta to the pulmonary arterial circulation will cause a drop in the diastolic pressure. The increase in blood return from the pulmonary veins into the left heart and aorta will cause elevation in systolic pressure. The result is an increased differ- ence between systolic and diastolic pressures or a widened pulse pressure. The precordium is hyperactive and a systolic thrill may be palpable in the left upper sternal region. An ejection murmur may be heard in infants due to elevated pulmonary vascular resistance at that age. A diastolic rumble may also be heard over the apical region due to the increase in blood return to the left heart and across the mitral valve. S1: first heart sound, S2: second heart sound, A: aortic valve closure, P: pulmonary valve closure. Due to the reduced blood volume in great vessels towards the end of diastole, blood flow is reduced just before the first heart sound and the murmur is not audible during late diastole. Patients with a large shunt will develop left atrial and ventricular dilatation causing an enlargement in the cardiac silhouette (Chap. A dilated left atrium should be suspected if there is a wide angle of bron- chial bifurcation at the carina and posterior deviation of the esophagus on lateral chest X-ray. Echocardiography Echocardiography is the procedure of choice to confirm the diagnosis. Cardiac Catheterization Cardiac catheterization is no longer necessary for diagnostic purposes. However, interventional cardiac catheterization is performed in most patients for therapeutic purposes. Eliminating the increased pulmonary blood flow helps to limit the pulmonary pathologies related to prematurity. Both indomethacin and ibuprofen have been used for their antagonizing effects on prostaglandins. The timing of closure depends on the size of the defect and the presence of symptoms. In asymptomatic infants, conservative management is possible to allow time for spontaneous closure. Placement of one or more coils in the ductus is usually sufficient to close small defects. In larger defects, an Amplatzer device, a cylindrical-shaped wire mesh plug, may be placed. The advantage of device closure is to avoid surgical thoracotomy; children can be discharged home the same day of procedure with good recovery. The complications may include residual leaks, coil embolization, hemolysis, pulmonary artery stenosis, or femoral vessel occlusion. Surgical closure is performed in cases not amenable to a percutaneous approach, such as young infants with congestive heart failure or pulmonary hypertension. Ligation and division of the ductus is usually performed through left thoracotomy. Complications may include bleeding, pneumothorax, infection and rarely, ligation of the left pulmonary artery or aorta. Patients with small defects have a normal prognosis apart from a small risk of developing endarteri- tis. In cases with a significant increase in pulmonary circulation and volume overload, there is a risk of congestive heart failure or irreversible pulmonary vas- cular disease. The pres- ence of respiratory distress syndrome may cause hypoxia and further promote ductal patency. Surfactant must be used cautiously in this population as it may rapidly lower pulmonary resistance causing an increase in left to right shunting. This is further complicated by an immature myocardium that may be unable to handle the volume overload. The physical examination reveals tachycardia, bounding peripheral pulses, a hyperactive precordium, and possibly a gallop rhythm on auscultation.

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Although sepsis should be a primary consideration order paroxetine 30mg free shipping, subtle signs suggestive of a cardiac anomaly should be noted buy 10mg paroxetine. The lack of apical impulse discount paroxetine american express, single second heart sound generic paroxetine 30mg mastercard, and significant oxygen desaturation beyond what is typically seen with sepsis, particularly in the absences of pulmonary disease findings on the chest X-ray, should prompt immediate investigation into cardiac causes. Other left sided obstructive lesions may also present with cardiac shock with a few notable differences. Subaortic obstruction due to ventricular septal hypertrophy will have a significant and harsh systolic ejection murmur and evidence of left ventricular hypertrophy on examination and electrocardiography. Severe coarctation of the aorta and interrupted aortic arch will have strong brachial arterial pulses with weak femoral pulses. Echocardiography should be done urgently in any case in which significant congenital heart disease is a possibility. Echocardiography will delineate the cardiac pathology as well as assess the size of any atrial communication and the patency of the ductus arteriosus. This child must be admitted to an intensive care unit for stabilization including fluid resuscitation, correction of metabolic acidosis, and initiation of prostaglandin infusion to maintain patency of the ductus arteriosus. The latter should be instituted even before diagnosis is confirmed as it will restore cardiac output and hasten stabilization. Busse Rashkind atrial septostomy must be performed if the atrial communication is restrictive. Stage I surgical repair (either Norwood of hybrid) can be delayed for a few days until the patient is clinically stable. As discussed, complete repair will require two additional procedures, typically performed at around 6 and 18 months of age. Case 2 A 32-year-old female at 38 weeks gestation presented in labor to a community hospital. Delivery was planned at a tertiary care center, but labor progressed rapidly and she came to the nearest hospital. The infant appeared to be stable at delivery with an oxygen saturation of 85% on room air. Communication with the pediatric cardiologist at the tertiary care center confirmed the diagnosis on record. The patient was transported to the tertiary care center in stable condition with no evidence of respiratory distress or metabolic acidosis. In view of the adequate atrial communication, it was felt that a Rashkind atrial septostomy was not necessary. A few hours after arrival, the child was noted to have apnea, a known complica- tion of prostaglandin infusion, and elective endotracheal intubation was performed. As previously discussed with parents, the child underwent a Norwood stage I surgical procedure at 1 week of life. Chapter 24 Ebstein’s Anomaly Russell Robert Cross and Ra-id Abdulla Key Facts • Ebstein’s anomaly of the tricuspid valve causes apical displacement of the effective orifice of the tricuspid valve resulting in large right atrium and smaller right ventricle. In severe cases the tricuspid valve is severely regurgitant and the right ventricular outflow tract is obstructed. These changes will lead to high right atrial pres- sure and right to left shunting at the foramen ovale leading to cyanosis. Definition Ebstein’s anomaly is a congenital heart disease affecting the tricuspid valve. In its milder form, the tricuspid valve is mildly displaced towards the apex with mild regurgitation and no stenosis. On the other hand, significant displacement of the tricuspid valve leaflets results in severe tricuspid valve regurgitation and lack of forward flow of blood in the right ventricu- lar outflow tract due to obstruction by the abnormal tricuspid valve. Cross and Ra-id Abdulla severe format of the disease develop significant escape of blood from the right atrium into the left atrium through right to left shunting, thus resulting in cyanosis. Patient with Ebstein’s anomaly are also known to have abnormal atrioventricular bridging of conductive tissue leading to preexcitaiton and tachyrhythmia. A small number of familial cases suggest that there could be a genetic linkage, but there is currently no specific mutation identified. There is some evidence to suggest an increased risk for Ebstein’s anomaly in the off-spring of women who are exposed to lithium during pregnancy, but this relationship has been disputed. Pathology It is primarily the septal and posterior leaflets of the tricuspid valve that are affected in Ebstein’s anomaly. The leaflets tend to have redundant tissue with short chordae and accessory attachments to the right ventricular septal surface, resulting in tethering of the leaflets to the septum. The tethering of the septal and posterior leaflets result in apical displacement of the tricuspid valve’s effective orifice into the right ventricular body so that the effective orifice no longer resides at the normal level of the atrio- ventricular groove. The apical displacement of the tricuspid valve results in an “atrialized” portion of the right ventricle, that is, part of the volume of the anatomic right ventricle becomes physiologically a component of the right atrium. Additionally, the wall of the atrialized portion of the right ventricle is thin, consistent with the lower pressures of the atrial chamber (Fig. Pathophysiology The tricuspid valve abnormalities seen in Ebstein’s anomaly create varying degrees of tricuspid insufficiency, right atrial enlargement, and right ventricular outflow tract obstruction. In milder forms of the disease, the tricuspid valve is not substan- tially displaced apically into the right ventricle. These patients usually have minimal tricuspid insufficiency and tend to have little in the way of symptoms. The tricuspid valve is apically displaced causing the right ventricle to be small and the right atrium to enlarge. Severe tricuspid regurgitation (white arrow) may cause the right atrium to further enlarge In more moderate forms of Ebstein’s anomaly, the tricuspid valve leaflets are positioned lower in the right ventricle resulting in greater degrees of tricuspid insuf- ficiency. Along with the tricuspid insufficiency there is increased right atrial enlargement. These individuals also may have right-to-left shunting of deoxy- genated blood at the level of the atrial septum through a patent foramen ovale or an atrial septal defect. The right to left shunting is a result of the tricuspid insufficiency and associated higher right atrial pressures, this results in cyanosis. Neonatal physiology in the more severe forms of Ebstein’s anomaly is domi- nated by severe tricuspid insufficiency and inability to create forward flow across the right ventricular outflow tract. The severe tricuspid insufficiency results in even greater right atrial enlargement, and makes it difficult for the right ventricle to create forward flow out the pulmonary artery. In some cases, the abnormal tricuspid valve leaflets can create a physical obstruction to flow across the right ventricular outflow tract. The situation may improve as pulmonary vascular resistance drops in the first several days of life, allowing more forward flow out the pulmonary artery. Cross and Ra-id Abdulla Presentation/Clinical Manifestations Infants with Ebstein’s anomaly typically have an unremarkable fetal course. Fetal echocardiography makes prenatal diagnosis possible, and allows for medical planning and early decision making in more severe forms of Ebstein’s anomaly. Newborn children with mild Ebstein’s anomaly often have no symptoms, but may have physical examination findings consistent with tricuspid insufficiency – a somewhat harsh, holosystolic murmur along the left lower sternal border. Moderate cases of Ebstein’s anomaly are associated with mild to moderate cyanosis resulting from the right-to-left atrial shunting, while more severe forms of Ebstein’s anomaly present in the neonatal period with significant cyanosis and evidence for conges- tive heart failure. A low cardiac output state may also exist in patients with severe Ebstein’s anomaly, resulting in poor perfusion and acidosis. Infants with moderate to severe Ebstein’s anomaly have increased right precor- dial activity and may have a right-sided heave. A third or fourth heart sound may also be present, creating the “quadruple gallop rhythm” associated with Ebstein’s anomaly. Older patients with Ebstein’s anomaly may present with supraventricular tachy- cardia. Ebstein’s anomaly is associated with Wolff–Parkinson–White syndrome (a type of electrical bypass tract) in 10–20% of patients. Additionally, patients with Ebstein’s anomaly may present later in life with symptoms of fatigue and exercise intolerance as a result of worsening heart failure associated with progressive tricuspid insufficiency and cardiac enlargement. Chest Radiography The chest X-ray in Ebstein’s anomaly is most notable for cardiomegally, the degree of which is related to the severity of tricuspid insufficiency. There may also be normal to decreased pulmonary vascular markings and a prominent right atrium (Fig. S1: first heart sound, S2: second heart sound, A: aortic valve closure, P: pulmonary valve closure. Severe tricuspid regurgitation may be audible as a holosystolic murmur heard best over the left lower sternal border 24 Ebstein’s Anomaly 287 Fig.

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As this process progresses order paroxetine 20mg amex, occlusion of perforating nutrient vessels to the skin causes progressive skin ischemia order generic paroxetine on line. As the condition evolves buy 10mg paroxetine amex, ischemic necrosis of the skin ensues with gangrene of subcutaneous fat purchase 40 mg paroxetine free shipping, dermis, and epidermis, manifesting progressively as bullae formation, ulceration, and skin necrosis (Fig. Margins of the skin are poorly defined with tenderness extending beyond the apparent area of involvement. Systemic manifestation such as fever, hypotension, and multiorgan failure can occur (50–53). The effects are classically caused by superantigen produced by group A Streptococcus. Total white cell count, hemoglobin, sodium, glucose, serum cretonne, and C-reactive protein were selected. The lack of bleeding may be seen or murky dishwater pus exudates may ooze from the incision site. The finger test can be used to delineate the extent of infection into the adjacent normal appearing skin. Repeated debridements may be required and should continue until the subcutaneous tissue can no longer be separated from the deep fascia. If infection progresses despite serial debridements and antibiotics, amputation may be life saving. Close monitoring of the physiology of the patient as well as serial laboratory data should be performed. A combination of broad-spectrum antibiotics, such as penicillin, and an aminoglycoside or a third-generation cephalosporin, and clindamycin or metronidazole can be started depending on the clinical presentation. Once the Gram stain culture and sensitivity results are obtained, the antibiotic regimen can be altered on the basis of these findings. One set of blood culture grew Gemella morbillorum and second set grew Streptococcus constellatus. Operative cultures obtained from left arm grew Klebsiella oxytoca, Peptostreptococcus micros, and Peptostreptococcus prevoti. Severe Skin and Soft Tissue Infections in Critical Care 305 Figure 6 Postoperative view in a diabetic patient with necrotizing fasciitis of right leg due to group G Streptococcus. Results are contradictory, with no real epidemiologically based studies performed (for treatment refer to Table 3). It is a fulminant, rapidly progressive subcutaneous infection of the scrotum and penis, which spreads along fascial planes and may extend to the abdominal wall. Fournier gangrene occurs commonly without a predisposing event or after uncomplicated hemor- rhoidectomy. Less commonly this can occur after urological manipulation or as a late complication of deep anorectal suppuration. Fournier gangrene is characterized by necrosis of the skin and soft tissues of the scrotum and/or perineum that is associated with a fulminant, painful, and severely toxic infection (58,59). Successful treatment is again based on early recognization and vigorous surgical debridement. Clostridial Myonecrosis (Gas Gangrene) Clostridium perfringens type A is the most common organism. Although initial growth of the organism occurs within the devitalized anaerobic milieu, acute invasion and destruction of healthy, living tissue rapidly ensues. Historically, clostridial myonecrosis was a disease associated with battle injuries, but 60% of cases now occur after trauma. It is a destructive infectious process of muscle associated with infections of the skin and soft tissue. It is often associated with local crepitus and systemic signs of toxemia, which are formed by anaerobic, gas-forming bacilli of the Clostridium sp. The infection most often occurs after abdominal operations on the gastrointestinal tract; however, penetrating trauma, and frostbite, can expose muscle, fascia, and subcutaneous tissue to these organisms. Common to all these conditions is an environment containing tissue necrosis, low-oxygen tension, and sufficient nutrients (amino acids and calcium) to allow germination of clostridial spores. Clostridia are gram-positive, spore-forming, obligate anaerobes that are widely found in soil contaminated with animal excreta. They may be isolated from the human gastrointestinal tract and from the skin in the perineal area. This organism produces collagenases and proteases that cause widespread tissue destruction, as well as a-toxin, which have a role in the high mortality associated with myonecrosis. The a-toxin causes extensive capillary destruction and hemolysis, leading to necrosis of the muscle and overlying fascia, skin, and subcutaneous tissues. Patients complain of sudden onset of pain at the site of trauma or surgical wounds, which rapidly increases in severity. Examination of the wound discharge reveals abundant large, boxcar-shaped gram-positive rods with a paucity of surrounding leukocytes. The usual incubation period between injury and the onset of clostridial myonecrosis is two to three days, but may be as short as six hours. A definitive diagnosis is based on the appearance of the muscle on direct visualization by surgical exposure. As the disease process continues, the muscle becomes frankly gangrenous, black, and extremely friable. Serum creatinine phosphokinase levels are always elevated with muscle involvement. Among the signs that predict a poor outcome are leukopenia, thrombocytopenia, hemolysis, and severe renal failure. Myoglobinuria is common and can contribute significantly to worsening of renal function. Frank hemorrhage may be present and is a harbinger of disseminated intravascular coagulation. Successful treatment of this life-threatening infection depends on early recogni- tion and debridement of all devitalized and infected tissues. The role of hyperbaric oxygen therapy has not been established (100% oxygen at 3 atm), but it may have a role early in the treatment of seriously ill patients (19,20). The mainstay of treatment is surgical debridement, and this should not be delayed. In this process, the bacterial tissue invasion is primarily superficial to the fascial layer, without muscle involvement. Prompt recognition and treatment, as described earlier, can reduce the associated morbidity and mortality. Protein synthesis inhibitors such as clindamycin when combined with penicillin has had considerable better efficacy than penicillin alone. Anaerobic streptococcal myonecrosis clinically resembles subacute clostridial gas gangrene. The involved muscles are discolored, in contrast to gas gangrene, early cutaneous erythema is prominent. The infection is usually mixed; anaerobic streptococci with group A Streptococcus or S. Treatment involves the use of high-dose penicillin and antistaphylococcal agent, if indicated, and surgical debridement. Cellulitis often develops within 12 to 24 hours, accompanied by excruciating pain, marked edema, and bullae. Infected vascular gangrene is a focal, usually indolent and primarily ischemic process in the small muscles of a distal lower extremity already gangrenous from arterial insufficiency. Diabetic patients are prone to develop this complication, which usually does not extend 308 Sharma and Saravolatz beyond the area of vascular gangrene to involve viable muscle. Bacterial infection of the muscle usually occurs after a penetrating wound, vascular insufficiency, or a contiguous spread. Common muscle involvement includes deltoid, psoas, biceps, gastrocnemius, gluteal, and quadriceps, though any muscle group can be involved. Patients will typically present with fever, pain, tenderness, and swelling of the involved muscle. Early modification of initial antimicrobial therapy is based on Gram stain and culture results. The most common lesion requiring hospitalization is the infected diabetic foot ulcer (Fig. Neuropathy plays a central role, with disturbances of sensory, motor, and autonomic functions leading to ulcerations due to trauma or excessive pressure on a deformed foot.

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Perhaps instead of being known throughout eternity as the betrayer of Jesus Christ order paroxetine 40 mg fast delivery, he might have become known as a great apostle cheap paroxetine online visa. This is possible because it was not necessary for Jesus to be betrayed by anyone in order to secure our salvation generic paroxetine 20mg on-line. It was His death and resurrection that saved us generic 20mg paroxetine fast delivery, and not the fact that He was betrayed by Judas. He spake of Judas Iscariot the son of Simon: for he it was that should betray him, being one of the twelve. He may have desperately cried out to the invisible God, bypassing the visible Christ. We make this same mistake when we cry out to the invisible God, and fail to confess our faults to the visible Christ. The imperfections of the visible body of Christ scares us out of confessing our sins. We tend instead to keep the sin a secret, and to privately try to work it out solely between God and us. Unfortunately, it’s often difficult to find a Christian to help us with our secret sins. Since Judas had never adequately dealt with this sin, his heart was fertile ground for a wicked seed-thought of betrayal to grow into an actual act of betrayal. We read of this germination process in John 13:2, “And supper being ended, the devil having now put into the heart of Judas Iscariot, Simon’s son, to betray him. It’s not the presence of an evil thought, but the submission to an evil thought that is sin. The process of thoughts turning into sins is broken down in James 1:14-15: “But every man is tempted, when he is drawn away of his own lust, and enticed. Then when lust hath conceived, it bringeth forth sin: and sin, when it is finished, bringeth forth death. Then if the door to the mind or body is opened by embracing the thought, a demon enters. As we study John 13, it appears that although Judas had apparently been a thief for a while, Jesus’ radical teachings on servanthood were pushing him to the crossroads of decision. Jesus shared some final words with them, and said, “If ye know these things, happy are ye if ye do them. I speak not of you all: I know whom I have chosen: but that the scripture may be fulfilled, He that eateth bread with me hath lifted up his heel against me…When Jesus had thus said, he was troubled in spirit, and testified, and said, Verily, verily, I say unto you, that one of you shall betray me. Had Judas been any less of an apostle, had he exhibited any less power or righteousness, all eyes would have turned to him. Judas was held in such high esteem by the other apostles that he wasn’t suspected. When Jesus whispered in John’s ear and strongly hinted that it was Judas, John refused to believe it. Satan was able to enter Judas because the apostle nurtured his own greed and embraced wicked thoughts. An invading demon either introduces wicked thoughts, or he magnifies the force of the intended victim’s own evil thoughts. The result is that thoughts that may have been dismissed before by an act of the person’s will, now are empowered by a demon. In the first example, a man who is otherwise faithful to his wife, secretly indulges in pornographic material. After a period of secret voluntary submission to his lust, he now finds it impossible to think of anything else except sex and committing adultery. In the next example, a suicidal teenager desperately wonders why he has had to fight homosexual thoughts all his life. He then comes to his senses and is horrified, or he is so tired of fighting that he accepts the lie that he was born a homosexual. Written on the dark caves of his tortured mind is the message: Better to yield to homosexuality than to lose my mind trying to fight it. As it so often happens in cases like these, a demon of suicide soon convinced him to escape the shame and pain by killing himself. Therefore it is written of a man who was an apostle among apostles: “Judas by transgression fell. We read: “But a certain man named Ananias, with Sapphira his wife, sold a possession, and kept back part of the price, his wife also being privy to it, and brought a certain part, and laid it at the apostles’ feet. But Peter said, Ananias, why hath Satan filled thine heart to lie to the Holy Ghost, and to keep back part of the price of the land? And Ananias hearing these words fell down, and gave up the ghost: and great fear came on all them that heard these things. And it was about the space of three hours after, when his wife, not knowing what was done, came in. Then Peter said unto her, How is it that ye have agreed together to tempt the Spirit of the Lord? Behold, the feet of them which have buried thy husband are at the door, and shall carry thee out. In our extremely sin tolerant culture, both in and out of the church, it is not popular to discuss divine judgment. Actually, according to the scripture judgment begins in the church before it reaches the world. And if the righteous scarcely be saved, where shall the ungodly and the sinner appear? The Spirit’s influence was so strong that it seems that the entire church, or at least a very large part of it, was caught up in sacrificial giving. Ananias and his wife wanted to participate in all the hoopla, but not in the same way. They conspired together to sell a possession, give some of the money to the church, and pretend that they had given all of it. Because whenever God’s power is mightily manifested in healing and deliverance, He also often manifests more immediate divine judgment upon those who are stumbling blocks to His work. Peter said to Ananias, “Why hath Satan filled thine heart to lie to the Holy Ghost? It means that He not only is in them, but that He is momentarily exercising a much greater degree of control over or through them than normal. Unknown to them, their plan to make themselves look better than they were had been inspired by a demon. This demon had filled their hearts in the same way that the Holy Spirit had filled the hearts of those whom they wanted to impress. Timothy and the Spirit of Fear This example may raise some eyebrows, but that’s okay. I only ask that you first of all remember that Bible characters were just as human as us. That means they were just as weak, just as inconsistent, just as fearful, just as frail, and just as sinful, as are we. It also means they were just as strong, just as consistent, just as courageous, and just as righteous, as are we. If we keep this in mind, we will not treat them as near gods and mar our understanding of the scriptures. This is why James said of the absolutely great prophet, Elijah, “Elias was a man subject to like passions as we are…. When you read the two short books that Paul wrote to Timothy, it is obvious that Timothy was not Paul. These scriptures will show you why I feel this way: “Let no man despise thy youth…Neglect not the gift that is in thee, which was given thee by prophecy, with the laying on of the hands of the presbytery. For God hath not given us the spirit of fear; but of power, and of love, and of a sound mind. Yet the circumstantial evidence is sufficient to build a case that this young preacher had a problem with a spirit of fear.

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