PATHOPHISIOLOGY OF CARDIOPULMONARY ARREST WHAT IS CARDIOPULMONARY ARREST?

Cardiac arrest, (also known as cardiopulmonary arrest or circulatory arrest) is the cessation of normal circulation of the blood due to failure of the heart to contract effectively. Medical personnel can refer to an unexpected cardiac arrest as a sudden cardiac arrest or SCA. A cardiac arrest is different from (but may be caused by) a heart attack, where blood flow to the muscle of the heart is impaired. Arrested blood circulation prevents delivery of oxygen to the body. Lack of oxygen to the brain causes loss of consciousness, which then results in abnormal or absent breathing. Brain injury is likely if cardiac arrest goes untreated for more than five minutes. For the best chance of survival and neurological recovery, immediate and decisive treatment is imperative.

Cardiac arrest is a medical emergency that, in certain situations, is potentially reversible if treated early. When unexpected cardiac arrest leads to death this is called sudden cardiac death (SCD). The treatment for cardiac arrest is cardiopulmonary resuscitation (CPR) to provide circulatory support, followed by defibrillation if a shockable rhythm is present. If a shockable rhythm is not present after CPR and other interventions, clinical death is inevitable.

MODIFIABLE: LIFESTYLE: No vices the family had a healthy lifestyle.

VIRAL DISEASE: causes

NON MODIFIABLE: NAME: Maurice Joseph, Enriques C. SEX: Male

BIRTHDATE: May 16, 2011 AGE: 2 months and 2 weeks NATIONALITY: Filipino

SIGNS AND SYMPTOMS

Cardiac arrest is an abrupt cessation of pump function in the heart (as evidenced by the absence of a palpable pulse). Prompt intervention can usually reverse a cardiac arrest, but without such intervention it will almost always lead to death.[1] In certain cases, it is an expected outcome to a serious illness. However, due to inadequate cerebral perfusion, the patient will be unconscious and will have stopped breathing. The main diagnostic criterion to diagnose a cardiac arrest, (as opposed to respiratory arrest which shares many of the same features), is lack of circulation, however there are a number of ways of determining this. Near death experiences are reported by 10-20% of people who survived cardiac arrest.

CAUSES
Coronary heart disease is the leading cause of sudden cardiac arrest. Many other cardiac and noncardiac conditions also increase ones risk. Coronary heart disease Approximately 6070% of SCD is related to coronary heart disease. Among adults, ischemic heart disease is the predominant cause of arrest with 30% of people at autopsyshowing signs of recent myocardial infarction. Non ischemic heart disease

A number of other cardiac abnormalities can increase the risk of SCD including: cardiomyopathy, cardiac rhythm disturbances, hypertensive heart disease, congestive heart failure. In a group of military recruits aged 1835, cardiac anomalies accounted for 51% of cases of SCD, while in 35% of cases the cause remained unknown. Underlying pathology included:coronary artery abnormalities (61%), myocarditis (20%), and hypertrophic cardiomyopathy (13%). Congestive heart failure increases the risk of SCD by 5 fold. Many additional conduction abnormalities exist that place one at higher risk for cardiac arrest. For instance, long QT syndrome, a condition often mentioned in young people's deaths, occurs in 1/5000-1/7000 newborns and is estimated to be responsible 3000 deaths each year compared to the approximately 300000 cardiac arrests seen by emergency services . These conditions are a fraction of the overall deaths related to cardiac arrest, but represent conditions which may be detected prior to arrest, which maybe treatable. Noncardiac SCDs is unrelated to heart problems in 35% of cases. The most common noncardiac causes: trauma, non-trauma related bleeding (such as gastrointestinal bleeding, aortic rupture, and intracranial hemorrhage), overdose, drowning and pulmonary embolism. Risk factors The risk factors for SCD are similar to those seen with coronary heart disease including: smoking, lack of physical exercise, obesity, diabetes, and family history. used to aid in remembering the possible treatable or reversible causes of cardiac arrest.

Hypovolemia - A lack of blood volume Hypoxia - A lack of oxygen Hydrogen ions (Acidosis) - An abnormal pH in the body Hyperkalemia or Hypokalemia - Both excess and inadequate potassium can be life-threatening. Hypothermia - A low core body temperature

Hypoglycemia or Hyperglycemia - Low or high blood glucose

Tablets or Toxins Cardiac Tamponade - Fluid building around the heart Tension pneumothorax - A collapsed lung Thrombosis (Myocardial infarction) - Heart attack Thromboembolism (Pulmonary embolism) - A blood clot in the lung Trauma

HIRSCHSPRUNG DISEASE
Hisrchsprung disease (HD) is Congenital megacolon HD is characterized by the absence of myenteric and submucosal ganglion cells in the distal alimentary tract; resulting in decreased motility in the affected bowel segment and loss of peristaltic activity distal to the area that is absent of ganglionc cells that leads to intestinal obstruction. Hirschsprung disease results from the absence of parasympathetic ganglion cells in the myenteric and submucosal plexus of the rectum and/or colon. Ganglion cells derived from the neural crest migrate caudally to anorectal area with the vagal nerve fibers along the intestine. Arrest in migration leads to an aganglionic segment. These ganglion cells arrive in the proximal colon by 8 weeks of gestational age and in the rectum by 12 weeks of gestational age.

Frequency: Approximately 1 per 5000 live births. Sex: 4 times more common in males than females. Age: Nearly all children nowadays with Hirschsprung disease are diagnosed during the first 2 years of life. One half are diagnosed before they are aged 1 year. Minority not recognized until later in childhood or adulthood. Mortality/Morbidity: The overall mortality of Hirschsprung enterocolitis is 25-30%, which accounts for almost all of the mortality from Hirschsprung disease. Classification: HD can be classified by the extension of the aganglionosis as follows: 1 Classical HD (75% of cases): Rectosegmoid area and distally to it will be aganglionic and its the most common type. 2- Long segment HD (20% of

cases): any part of the colon beyond the recto sigmoid area is affected. (More than half of the colon -DHMC) 3- Total colonic aganglionosis (3-12% of cases): the terminal ileum will be aganglionic and distally to it. 4- Rare variants include the following: Total intestinal aganglionosis: its incompatible with life because the whole GI tract dont have ganglion. Ultra-short-segment HD: involving the distal rectum below the pelvic floor and the anus. Extra: the aganglionic segment in ultra short is limited to internal sphincter, ganglion cells present on rectal suction biopsy but rectal motility is abnormal. Clinical presentation: Most of the patients diagnosed at first month so in the: Newborns: 1-Failure to pass meconium within the first 48 hours of life (meconium is a green blackish first stool that the child passes and at first 24 to 48 hours), and 95% of HD patients have delay in passging the stool. 2-Abdominal distension that is relieved by rectal stimulation (then the mother inserts rectal thermometer to take temp or enema, she notes that the child will pass stool after a while) 3-if the child wasnt diagnosed early he will complain of serious intestinal obstruction like vomiting fecal material, sever dehydration and rarely enterocolitis and the mortality rate is 20-30 % without treatment but with, it will reach 100%. 4-failure to thrive (the normal gaining weight is 25 gm/day) Older children and adults Severe constipation Abdominal distension Bilious vomiting Failure to thrive Diagnostic workup Clinically: we take a good history we see an abdominal distention, then we do a rectal examination and we see that there is stool on the finger because when we do PR we make relaxation of the internal sphincter, and some of the stool or gas will come out. Investigations: 1- Plain abdominal x-ray: we see distended colon because of the obstruction, and lately the small bowl will be distended either. 2- Contrast enema: barium or gastrografin enema, we see: A transitional zone will appear between the normal bowl and the abnormal one. Abnormal, irregular contractions of aganglionic segment. Delayed evacuation of barium (so even taking image after 24 h will show that barium is still there). 3- Manometry: its like a defecation reflex, normally the colon contains the stool and the rectum is empty, so when we defecate the stool goes to the rectum. The idea is we put a ballon in the rectum and we inflate it, and we put a manometer in the anal sphincter. Normally when the ballon is inflated the sphincter relaxes. In HD patients the anal sphincter remains contracted because absence of ganlionic cells.

4- Biopsy: we take biopsy from the rectum to the histopathology lab to see if there any ganglionic cells or not. one ganglionic cell is sufficient to exclude HD. Types: Treatment rectal suction biopsy ( here we take mucosa and sometimes submucosa) Full-thickness rectal biopsy. The treatment is surgical removal or bypass of the aganglionic bowel with preservation of the sphincter because we dont want to end with incontinence. Complications -HD associated enteropathy: its exactly like the gastroenteritis that happens in children which is very common. Because of the stagnation of the stool, bacterial overgrowth will occur and starts to secrets toxins, besides that the mucosa isnt healthy which finally lead to early sepsis. -So the patient will come firstly with fever, abdominal distention, and even diarrhea (the diarrhea here because of the overflow that resulted from the inflammatory process and secretions from the colon), lethargy (drowsiness), rectal bleeding, or shock. So the patient will rapidly deteriorate because of sepsis and dehydration. -Mortality rate is with treatment is 20%. -Treatment: rehydration,IV antibiotics,colonic washout to treat the primary cause which is stool stagnation. Prognosis Usually they complain of constipation, because of not extracting all aganglionic cells in surgery, so we give those suppositories, enemas, lactulose. But in general they live normally. Some investigators report a high degree of satisfaction, while others report a significant incidence of constipation and incontinence. Approximately 1% of patients with Hirschsprung disease require a permanent colostomy to correct incontinence. Patients with associated trisomy 21 have poorer clinical outcomes. ANORECRAL MALFORMATIONS Imperforate anus: The child comes without anus or obstructed anus, frequency: 1 per 5000 live births And it can be: Low type: (anal problem, anal agensis,anal malformation),less severe, outcome almost normal after treatment. The presence of meconium at the perineum,it means that there is a way out,so the meconium can go out from the anus,or from a fistula that presents at the mid spot(its like a canal from the anus to the scrotum). Bucket-handle visible).

A bucket-handle malformation, its like bridge. Anal membrane (through which meconium is visible) Treatment: dilating the existing opening (anoplasty). High type: more severe, outcome poor, incontinence because the sphincter is not developed. A flat perineum (the lack of a midline gluteal fold). Absence of an anal dimple (visible indentations of the skin,), indicates that the patient has poor muscles in the Treatment: it's more difficult because the colon below the sphincter is atretic (not existed), so we have to open a way through the sphincter to the skin outside, and its complicated with fibrosis and infection, so we do colostomy temporarily to have a chance to clean out the stool below the sphincter so the surgery will be less complicated and lesser damage to the sphincter.