Let us consider a ferromagnetic material which is subjected to magnetizing field (H). The intensity of the magnetizing field (H) is gradually increased from 0. Then, the magnetic induction (B) also increases and becomes maximum (at point L in the graph). This state is called magnetic saturation.

On decreasing the value of magnetizing field (H), the magnetic induction (B) also decreases but the path that it follows is not the same. When magnetizing field (H) becomes 0, magnetic induction (B) doesn’t come down to 0 (the material is still magnetized). The value of magnetic induction (B) at which the magnetizing field (H) is equal to 0 is called retentivity or remanence of the material.

On decreasing magnetizing field (H) further from 0 (applying magnetizing field in opposite direction), magnetic induction (B) in the material decreases further and it becomes 0 (demagnetized) at certain value of magnetizing field (H). This value is called coercivity of the material.

On further decrement in the value of magnetizing field (H), the magnetization of the material is reversed and it saturates in the opposite direction (at point E in the graph).

Similarly, if the value of magnetizing field (H) is reduced to 0, the retentivity field appears in the material at point F. Again, on reversing the direction of the field, the material is completely demagnetized at point G (coercivity field). Then the material is again magnetized in positive direction and it once again gets saturated. This completes the cycle of alternating magnetization of the material and the curve repeats in other cycle.

In the process of alternating magnetization of the magnetic material, it is seen that magnetic induction (B) lags behind magnetizing field (H). This phenomenon in which the magnetic induction (B) lags behind magnetizing field (H) is called magnetic hysteresis. The B-H curve for one complete cycle is called hysteresis loop of the material. The area covered by the hysteresis loop represents the loss of energy within the material when it is magnetized and demagnetized. The loss of energy is called hysteresis loss and it is in the form of heat energy.

 Peritonitis is the inflammation of the peritoneum or peritoneal membrane. The peritoneum is a semi-permeable membrane two layered sac filled about 1500ml of fluid. This sac covers all the organs in the abdominal cavity. Because it is well supplied with the somatic nerves, stimulation of the parietal peritoneum that lines the abdominal and pelvic cavities causes sharp & localized pain. The visceral peritoneum is relatively insensitive.

Etiology/ Risk factors/ causative factors:

• Major sources of inflammation are from GI tract, external environment and through blood stream.
• Normal flora of the intestine becomes a source of infection when they enter the sterile peritoneal cavity.
• Most common causative organisms are,
• E. coli
• Streptococci
• Staphylococci
• Pneumococci
• Gonococci
• Ruptured or gangrenous gall bladder.
• Perforated peptic ulcer, perforated stomach or intestine secondary to cancer or inflammatory bowel disorders, bowel obstruction, penetrating wounds.
• Other conditions- Acute pancreatitis & mesenteric thrombosis.
• Caused by chemical response to irritating substances such as might occur following rupture of fallopian tube, in an ectopic pregnancy, perforation of a Gastric ulcer or traumatic rupture of the spleen or liver.

## Patho-physiology for Peritonitis:

Peritonitis produces severe systemic effects. Circulatory alterations, fluid shifts & respiratory problems can cause critical fluid and electrolyte imbalance. Inflammatory response shunts (diverts) extra blood to the inflamed area ot the bowel to combat infection. Peristaltic activity of the bowel stops (ceases). Fluid and air are retained in its lumen raising pressure & increasing fluid secretion into the bowel. Circulatory blood volume diminishes. Inflammatory process increases oxygen requirement at a time when the client has difficulty ventilating (co’z of abd. pain abd. pressure, w! elevates the diaphragm).

Clinical Manifestations:
Varies according to the causes:

• Pain – sudden diffuse, severe abdominal pain that tends to intensify & localize in the area of the underlying cause or disorder with associated rebound tenderness.
• Weakness and pallor.
• Excessive sweating (diaphoresis)
• Cold skin
• Decreased intestinal motility & paralytic ileuses (Assessment reveals)
• Hypotension
• Fever (low grade)
• Abdominal distention
• Nausea/ vomiting
• Shallow respiration
• Hypovolemia & finally shock

Diagnostic Findings for Peritonitis:

• History taking
• Physical examination reveals; Absence of bowel sounds & shallow respiration
Laboratory investigations
• Blood – WBC # 20,000/mm3 (leucocytosis)
– Neutrophils #
• Abdominal x-ray – reveals dilation & edema of the intestine or free air or fluid in the abdominal cavity or in the case of visceral organ perforation, air lying under the diaphragm.
• Manifestations of imbalanced fluid and electrolyte balance may present.
• Chest x-ray may show elevation of the diaphragm.
• Paracentesis reveals bacteria, exudates, blood, pus or urine.

## Management for Peritonitis:

Aim

•   To combat infection
• Restore intestinal motility
• Supply lost.

i) Medical management:

•  Maintain fluid and electrolyte balance.
• Oral fluids are prohibited
• IV fluids are necessary for the replacement of electrolyte and protein losses.
• NG tube is inserted to reduce pressure within the bowel.

Control infection

• Once the infection has been walled off and the clients condition improves, surgical drainage repair can be attempted.
• Massive doses of antibiotics are administered parenterally. (i.e. Potent broad spectrum agents)

ii) Surgical management:

• Exp.(explorative) ‘laparatomy’

iii) Nursing management:
Pre-operative:

• Obtain a thorough history, including specific information about the clients pain. Assess the abdomen, nothing the presence of bowel sound or its absence. Palpate the abd. for firm, distended or rigid. Note the areas of tenderness.
• Massive doses of antibiotics are administered parentarally. (because clients of peritonitis are acutely ill)
• Intestinal & gastric incubation is usually ordered at once, the tubes are attached to suction (decompression of the stomach)
• NPO
• I/V therapy
• Narcotics & sedatives are given for severe pain & apprehension as soon as the diagnosis is confirmed and there is no danger of making symptoms.
• Patient placed in semi-fowler’s position (gravity may help localize pus in the lower abdomen or the pelvis.
• Patient prepared for emergency surgery.
• The perforated organs are usually repaired as soon as the client is stable enough to withstand the stress of surgery.
• During surgery any leakage can be sampled for culture so that specific antibiotic therapy can be implemented.

Post-operative:

• Carefully monitor clients for the development of post-operative complications such as ARDS, sepsis and shock.
• Closely monitor the vital signs and record it.
• Closely monitor the client’s fluid balance by assessing vital signs, bowel sounds, urine output, skin turgor, mucus membrane, weight.
• Immediately report any manifestations of sepsis, such as drop in B.P. rise in temperature, clean sterile dressings.
• I/v fluids replacement & parentally antibiotics as prescribed.
• On discharge provide the client i.e., oral or written instructions regarding wound care medication actively restrictions and follow up visits.