VELEZ COLLEGE

COLLEGE OF NURSING

A CASE STUDY ON PATIENT R.G, 11 YRS OLD, MALE, DIAGNOSED WITH CARDIOPULMONARY ARREST SECONDARY TO SEVERE METABOLIC ACIDOSIS SECONDARY TO END STAGE
RENAL DISEASE SECONDARY TO CHRONIC PYELONEPHRITIS, ASPIRATION PNEUMONIA, CERBRAL PALSY S/P TENCKHOFF CATHETER INSERTION

SUBMITTED TO:
MS. ANNE B. EMBRADURA

SUBMITTED BY:
BSN IV
Alcordo, Necille Ann Marie
Diorico, Christian
Largo, Tresha
Santiago, Hannah

BSN III
Abrenica, Karen
Maratas, Den Zachary
Ramos, Marra
San Pedro, Joannah Joy

BSN II
Albao, Cielo
Aldaya, Aprelle Angeli
Cortes, Ma. Carmela Angela
Desquitado, Christian Randolph
Espina, Ma. Angelica
Lanaria, Kevin Caile
Pepito, Hannah Jill
Tan, Richard

R.G., 11 years old, male, Roman Catholic, from Ticad, Bantayan Island, Cebu, was admitted for the first time at Cebu Velez General Hospital on September 30, 2009 via ambulance from Chong Hua
Hospital, accompanied by mother and grandmother for complaints of difficulty breathing noted about 1 month PTA and recurred 2 days PTA. Patient was admitted under the services of Dr. Monina
Christina Cabral of the Department of Pediatrics with a case number of 06750 and a hospital number of 082047.
CEREBRAL PALSY
Cerebral Palsy is an umbrella term encompassing a group of non-progressive, motor, non-contagious conditions that cause physical disability in human development. This is caused by damage to
the motor control centers of the developing brain and can occur during pregnancy (about 75 percent), during childbirth (about 5 percent) or after birth (about 15 percent) up to about age three. Further
research is needed on adults with CP as the current literature is highly focused on the pediatric patient.
Cerebral palsy describes a group of permanent disorders of the development of movement and posture, causing activity limitation, that are attributed to nonprogressive disturbances that occurred in
the developing fetal or infant brain. The motor disorders of cerebral palsy are often accompanied by disturbances of sensation, perception, cognition, communication, and behavior, by epilepsy, and
by secondary musculoskeletal problems.
Classification:
CP is divided into three major classifications to describe different movement impairments. These classifications also reflect the areas of the brain that are damaged. The three major classifications
are:
a. Spastic
Spastic cerebral palsy is by far the most common type, occurring in 70% to 80% of all cases. People with this type are hypertonic and have a neuromuscular condition stemming from
damage to the corticospinal tract or the motor cortex that affects the nervous system's ability to receive gamma amino butyric acid in the area(s) affected by the disability. Spastic CP is
further classified by topography dependent on the region of the body affected; these include:
Spastic hemiplegia (one side being affected). Generally, injury to muscle-nerves controlled by the brain's left side will cause a right body deficit, and vice versa. Typically, people
that have spastic hemiplegia are the most ambulatory, although they generally have dynamic equinus on the affected side and are primarily prescribed ankle-foot orthoses to
prevent said equinus.
Spastic diplegia (the lower extremities are affected with little to no upper-body spasticity). The most common form of the spastic forms. Most people with spastic diplegia are fully
ambulatory and have a scissors gait. Flexed knees and hips to varying degrees are common. Hip problems, dislocations, and in three-quarters of spastic diplegics, also
strabismus (crossed eyes), can be present as well. In addition, these individuals are often nearsighted. The intelligence of a person with spastic diplegia is unaffected by the
condition.
Spastic tetraplegia (all four limbs affected equally). People with spastic quadriplegia are the least likely to be able to walk, or if they can, to want to walk, because their muscles are
too tight and it is too much effort to do so. Some children with quadriplegia also have hemiparetic tremors, an uncontrollable shaking that affects the limbs on one side of the body
and impairs normal movement.
Occasionally, terms such as monoplegia, paraplegia, triplegia, and pentaplegia may also be used to refer to specific manifestations of the spasticity.
b. Ataxic
Ataxia type symptoms can be caused by damage to the cerebellum. The forms of ataxia are less common types of cerebral palsy, occurring in at most 10% of all cases. Some of these
individuals have hypotonia and tremors. Motor skills such as writing, typing, or using scissors might be affected, as well as balance, especially while walking. It is common for individuals to
have difficulty with visual and/or auditory processing.
c. Athetoid/dyskinetic
Athetoid or dyskinetic is mixed muscle tone and sometimes hypotonia (Hypotonia will usually occur before 1 year old; the muscle tone will be increased with age and progress to
Hypertonia). People with athetoid CP have trouble holding themselves in an upright, steady position for sitting or walking, and often show involuntary motions. For some people with athetoid
CP, it takes a lot of work and concentration to get their hand to a certain spot (like scratching their nose or reaching for a cup). Because of their mixed tone and trouble keeping a position,
they may not be able to hold onto objects (such as a toothbrush or pencil). About one quarter of all people with CP have athetoid CP. The damage occurs to the extrapyramidal motor system
and/or pyramidal tract and to the basal ganglia. It occurs in 40 percent of all cases. In newborn infants, high bilirubin levels in the blood, if left untreated, can lead to brain damage in certain
areas. This may also lead to athetoid cerebral palsy.

Symptoms:
All types of CP are characterized by abnormal muscle tone, reflexes, or motor development and coordination. There can be joint and bone deformities and contractures. The classical symptoms
are spasticities, spasms, other involuntary movements, unsteady gait, problems with balance, and/or soft tissue findings consisting largely of decreased muscle mass. Scissor walking and toe walking
are common among people with CP who are able to walk, but taken on the whole, CP symptomatology is very diverse. The effects of cerebral palsy fall on a continuum of motor dysfunction which
may range from slight clumsiness at the mild end of the spectrum to impairments so severe that they render coordinated movement virtually impossible at the other end the spectrum.
Babies born with severe CP often have an irregular posture; their bodies may be either very floppy or very stiff. Birth defects, such as spinal curvature, a small jawbone, or a small head
sometimes occur along with CP. Symptoms may appear or change as a child gets older. Some babies born with CP do not show obvious signs right away. Classically, CP becomes evident when the
baby reaches the developmental stage at 6-9 months and is starting to mobilize, where preferential use of limbs, asymmetry or gross motor developmental delay is seen.
Speech and language disorders are common in people with Cerebral Palsy. Speech problems are associated with poor respiratory control, laryngeal and velopharyngeal dysfunction as well as
oral articulation disorders that are due to restricted movement in the oral-facial muscles. There are three major types of dysarthria in cerebral palsy: spastic, dyskinetic (athetosis) and ataxic. Speech
impairments in spastic dysarthria involves four major abnormalities of voluntary movement: spasticity, weakness, limited range of motion and slowness of movement. Speech mechanism impairment
in athetosis involves a disorder in the regulation of breathing patterns, laryngeal dysfunction (monopitch, low, weak and breathy voice quality). It is also associated with articulatory dysfunction (large
range of jaw movements), inappropriate positioning of the tongue, instability of velar elevation. Athetoid dysarthria is caused by disruption of the internal sensorimotor feedback system for appropriate
motor comands, which leads to the generation of faulty movements that are perceived by others as involuntary. Ataxic dysarthria is uncommon in cerebral palsy. The speech characteristics are:
imprecise consonants, irregular articulatory breakdown, distorted vowels, excess and equal stress, prolonged phonemes, slow rate, monopitch, monoloudness and harsh voice.
Causes:
While in certain cases there is no identifiable cause, other etiologies include problems in intrauterine development, asphyxia before birth, hypoxia of the brain, and birth trauma during labor and
delivery, and complications in the perinatal period or during childhood. CP is also more common in multiple births.
Studies at the University of Liverpool have led to the hypothesis that many cases of cerebral palsy, and other conditions that an infant has at birth, are caused by the death in very early
pregnancy of an identical twin. This may occur when twins have a joint circulation through sharing the same placenta. Not all identical twins share the same blood supply (monochorionic twins), but if
they do, the suggestion is that perturbations in blood flow between them can cause the death of one and damage to the development of the surviving fetus. It is common knowledge amongst
obstetricians and midwives that a small dead fetus (fetus papyraceus) may sometimes be found attached to a placenta following birth. In the past, this has not been considered important and
knowledge of the so called vanishing twin has been suppressed to avoid triggering feelings of loss, grief, or guilt in mothers. The pathological consequences depend on the severity and the stage of
development of the fetus when the imbalances in blood flow between the fetuses occur. It has been proposed that such pathology could account, not just for cerebral palsy, but for developmental
abnormalities of the eye, heart, and gut, and other specific brain abnormalities such as neuronal migration disorders, which occur during very early fetal development.
Between 40% and 50% of all children who develop cerebral palsy were born prematurely. Premature infants are vulnerable, in part because their organs are not fully developed, increasing the
risk of hypoxic injury to the brain that may manifest as CP. A problem in interpreting this is the difficulty in differentiating between CP caused by damage to the brain that results from inadequate
oxygenation and CP that arises from prenatal brain damage that then precipitates premature delivery.
Recent research has demonstrated that intrapartum asphyxia is not the most important cause, probably accounting for no more than 10 percent of all cases; rather, infections in the mother, even
infections that are not easily detected, may triple the risk of the child developing the disorder, mainly as the result of the toxicity to the fetal brain of cytokines that are produced as part of the
inflammatory response.
Low birthweight is a risk factor for CPand premature infants usually have low birth weights, less than 2.0 kg, but full-term infants can also have low birth weights.
Multiple-birth infants are also more likely than single-birth infants to be born early or with a low birth weight.
After birth, other causes include toxins, severe jaundice, lead poisoning, physical brain injury, shaken baby syndrome, incidents involving hypoxia to the brain, and encephalitis or meningitis. The
three most common causes of asphyxia in the young child are: choking on foreign objects such as toys and pieces of food, poisoning, and near drowning.
Diagnosis:
The diagnosis of cerebral palsy has historically rested on the patient's history and physical examination. Once diagnosed with cerebral palsy, further diagnostic tests (MRI, CT scan) are optional.
Treatment:
There is no cure for CP, but various forms of therapy can help a person with the disorder to function and live more effectively. Treatment is usually symptomatic and focuses on helping the
person to develop as many motor skills as possible or to learn how to compensate for the lack of them. In general, the earlier treatment begins the better chance children have of overcoming

developmental disabilities or learning new ways to accomplish the tasks that challenge them. Treatment may include one or more of the following: physical therapy; occupational therapy; speech
therapy; drugs to control seizures, alleviate pain, or relax muscle spasms (e.g. benzodiazepienes, baclofen and intrathecal phenol/baclofen); hyperbaric oxygen; the use of Botox to relax contracting
muscles; surgery to correct anatomical abnormalities or release tight muscles; braces and other orthotic devices; rolling walkers; and communication aids such as computers with attached voice
synthesizers.
Surgery for people with CP usually involves one or a combination of:
Loosening tight muscles and releasing fixed joints, most often performed on the hips, knees, hamstrings, and ankles. In rare cases, this surgery may be used for people with stiffness of their
elbows, wrists, hands, and fingers.
The insertion of a Baclofen Pump usually during the stages while a patient is a young adult. This is usually placed in the left abdomen. It is a pump that is connected to the spinal cord,
whereby it sends bits of Baclofen alleviating the continuous muscle flexion. Baclofen is a muscle relaxant and is often given PO to patients to help counter the effects of spasticity.
Straightening abnormal twists of the leg bones, i.e. femur (termed femoral anteversion or antetorsion) and tibia (tibial torsion). This is a secondary complication caused by the spastic muscles
generating abnormal forces on the bones, and often results in intoeing (pigeon-toed gait). The surgery is called derotation osteotomy, in which the bone is broken (cut) and then set in the
correct alignment.
Cutting nerves on the limbs most affected by movements and spasms. This procedure, called a rhizotomy, "rhizo" meaning root and "tomy" meaning "a cutting of" from the Greek suffix 'tomia'
reduces spasms and allows more flexibility and control of the affected limbs and joints.
Botulinum Toxin A (Botox) injections into muscles that are either spastic or have contractures, the aim being to relieve the disability and pain produced by the inappropriately contracting
muscle.
A new study has found that cooling the bodies and blood of high-risk full-term babies shortly after birth may significantly reduce disability or death.
Cord Blood Therapy: There are no published randomized controlled trials or meta-analysis of this treatment modality in cerebral palsy. In March 2008 a boy diagnosed with cerebral palsy appeared
on the Today Show with his family.[41] The parents noted that he could not walk on his own and appeared to be "swallowing his tongue" at times. He was eventually diagnosed with cerebral palsy and
could only walk with the aid of a walker for a short time. Earlier that year he participated in a clinical trial involving his own cord blood that his parents had saved when he was born. His parents
reported that within 5 days after the procedure he was walking on his own and talking, something his mother said he was not capable of on his own and it was doubtful he would ever be able to do on
his own. They also reported that the doctors also told them that if his rate of progress continues uninterrupted until he is 7 he will be pronounced cured.

PYELONEPHRITIS
Pyelonephritis is an inflammation of the renal pelvis and parenchyma caused by bacterial infection. The cause may be an active infection in the kidney or the remnants of a previous infection in the
kidney or the remnants of a previous infection.
Cause:
Ureteral reflux, which allows infected urine back into the ureter, and obstruction, which causesto back into the ureter and allows microorganisms to multiply, are the most common causes of
pyelonephriris. Common organisms are E. coli (70-80%) and Enterococcus faecalis. Most cases of pyelonephritis start off as lower urinary tract infections, mainly cystitis and prostatitis.
Risk is increased in the following situations:
Constitutional: diabetes mellitus, immunocompromised states
Positive family history (close family members with frequent urinary tract infections)
Signs and symptoms:
Acute pyelonephritis is characterized by enlarged kidneys, focal parenchymal abscesses. Assessment usually reveals high fever, chills, nausea, flank pain on the affected side,
headache and muscle pain. The pain commonly radiates down the ureter or toward the epigastrium. Dysuria, frequency and urgency are commonly experienced. The urine may
also be cloudy or bloody, foul-smelling and shows a marked increase in WBCs and casts.
On the other hand, chronic pyelonephritis has no specific manifestations of its own. Hypertension is the most frequent manifestation of the disease.

Diagnosis:
Urinalysis: The presence of nitrite and leukocytes (white blood cells) on urine in patients with typical symptoms are sufficient for the diagnosis of pyelonephritis.
Formal diagnosis is with culture of the urine; blood cultures may be needed if the source of the infection is initially doubtful.
Treatment:
As practically all cases of pyelonephritis are due to bacterial infections, antibiotics are the mainstay of treatment. Mild cases may be treated with oral therapy, but generally intravenous antibiotics
are required for the initial stages of treatment. The type of antibiotic depends on local practice, and may include fluoroquinolones beta-lactam antibiotics, trimethoprim.
Some recommend other nutritional approaches to prevent recurrence of UTIs. Increasing fluid intake, consuming cranberry juice, blueberry juice, and fermented milk products containing probiotic
bacteria, have been shown to inhibit adherence of bacteria to the epithelial cells of the urinary tract.
Renal damage can cause hypertension thus it is important to control increase in BP. Reduction of dietary sodium and pharmacologic therapy may be indicated.

CHRONIC RENAL FAILURE

Chronic kidney disease (CKD), also known as chronic renal disease, is a progressive loss of renal function over a period of months or years. The symptoms of worsening kidney function are
unspecific, and might include feeling generally unwell and experiencing a reduced appetite. Often, chronic kidney disease is diagnosed as a result of screening of people known to be at risk of kidney
problems, such as those with high blood pressure or diabetes and those with a blood relative with chronic kidney disease. Chronic kidney disease may also be identified when it leads to one of its
recognized complications, such as cardiovascular disease, anemia or pericarditis.
Signs and symptoms:
Initially it is without specific symptoms and can only be detected as an increase in serum creatinine or protein in the urine. As the kidney function decreases:
blood pressure is increased due to fluid overload and production of vasoactive hormones, increasing one's risk of developing hypertension and/or suffering from congestive heart failure
Urea accumulates, leading to azotemia and ultimately uremia. Urea is excreted by sweating and crystallizes on skin (uremic frost).
Potassium accumulates in the blood (known as hyperkalemia with a range of symptoms including malaise and potentially fatal cardiac arrhythmias)
Erythropoietin synthesis is decreased (potentially leading to anemia, which causes fatigue)
Fluid volume overload - symptoms may range from mild edema to life-threatening pulmonary edema
Hyperphosphatemia - due to reduced phosphate excretion, associated with hypocalcemia (due to vitamin D3 deficiency). The major sign of hypocalcemia being tetany.
o Later this progresses to tertiary hyperparathyroidism, with hypercalcaemia, renal osteodystrophy and vascular calcification that further impairs cardiac function.
Metabolic acidosis, due to accumulation of sulfates, phosphates, uric acid etc. This may cause altered enzyme activity by excess acid acting on enzymes and also increased excitability of
cardiac and neuronal membranes by the promotion of hyperkalemia due to excess acid
People with chronic kidney disease suffer from accelerated atherosclerosis and are more likely to develop cardiovascular disease than the general population. Patients afflicted with chronic
kidney disease and cardiovascular disease tend to have significantly worse prognoses than those suffering only from the latter.
Diagnosis:
Chronic kidney disease is identified by a blood test for creatinine. Higher levels of creatinine indicate a falling glomerular filtration rate and as a result a decreased capability of the kidneys to
excrete waste products. Creatinine levels may be normal in the early stages of CKD, and the condition is discovered if urinalysis (testing of a urine sample) shows that the kidney is allowing the loss
of protein or red blood cells into the urine.
To fully investigate the underlying cause of kidney damageblood tests and often renal biopsy (removing a small sample of kidney tissue) are employed to find out if there is a reversible cause for
the kidney malfunction. Additional tests may include nuclear medicine MAG3 scan to confirm blood flows and establish the differential function between the two kidneys. DMSA scans are also used in
renal imaging; with both MAG3 and DMSA being used chelated with the radioactive element Technetium-99.
Stages:

All individuals with a Glomerular filtration rate (GFR) <60 mL/min for 3 months are classified as having chronic kidney disease, irrespective of the presence or absence of kidney damage. The
rationale for including these individuals is that reduction in kidney function to this level or lower represents loss of half or more of the adult level of normal kidney function, which may be associated
with a number of complications.
Stage 1 CKD
Signs of mild kidney disease but with normal or better GFR (>90 mL/min)
Stage 2 CKD
Mild kidney disease with reduced GFR (60-89 mL/min)
Stage 3 CKD
Moderate chronic renal insufficiency (30-59 mL/min)
Stage 4 CKD
Severe chronic renal insufficiency (15-29 mL/min)
Stage 5 CKD
End-stage renal failure (GFR <15 mL/min)
Causes:
The most common causes of CKD are diabetic nephropathy, hypertension, and glomerulonephritis. Together, these cause approximately 75% of all adult cases. Certain geographic areas have a high
incidence of HIV nephropathy.
Historically, kidney disease has been classified according to the part of the renal anatomy that is involved, as:
Vascular, includes large vessel disease such as bilateral renal artery stenosis and small vessel disease such as ischemic nephropathy, hemolytic-uremic syndrome and vasculitis
Glomerular, comprising a diverse group and subclassified into
o Primary Glomerular disease such as focal segmental glomerulosclerosis and IgA nephritis
o Secondary Glomerular disease such as diabetic nephropathy and lupus nephritis
Tubulointerstitial including polycystic kidney disease, drug and toxin-induced chronic tubulointerstitial nephritis and reflux nephropathy
Obstructive such as with bilateral kidney stones and diseases of the prostate
Treatment:
The goal of therapy is to slow down or halt the otherwise relentless progression of CKD to stage 5. There is no specific treatment unequivocally shown to slow the worsening of chronic kidney
disease. If there is an underlying cause to CKD, such as vasculitis, this may be treated directly with treatments aimed to slow the damage. In more advanced stages, treatments may be required for
anemia and bone disease. Severe CKD requires one of the forms of renal replacement therapy; this may be a form of dialysis, but ideally constitutes a kidney transplant.
Replacement of erythropoietin and vitamin D3, two hormones processed by the kidney, is usually necessary in patients with CKD, as is calcium. Phosphate binders are used to control the serum
phosphate levels, which are usually elevated in chronic kidney disease.
In some cases, dietary modifications have been proven to slow and even reverse further progression. Generally this includes limiting a persons intake of protein.

PERITONEAL DIALYSIS
Peritoneal dialysis (PD) is a treatment for patients with severe chronic kidney failure. The process uses the patient's peritoneum in the abdomen as a membrane across which fluids and dissolved
substances (electrolytes, urea, glucose, albumin and other small molecules) are exchanged from the blood. Fluid is introduced through a permanent tube in the abdomen and flushed out either every
night while the patient sleeps (automatic peritoneal dialysis) or via regular exchanges throughout the day (continuous ambulatory peritoneal dialysis). PD is used as an alternative to hemodialysis
though it is far less common. It has comparable risks and expenses, with the primary advantage being the ability to undertake treatment without visiting a medical facility. The primary complication
with PD is a risk of infection due to the presence of a permanent tube in the abdomen.

Method
The abdomen is cleaned in preparation for surgery, and a catheter is surgically inserted with one end in the abdomen and the other protruding from the skin. Before each infusion the area must be
cleaned, and flow into and out of the abdomen tested. A large volume of fluid is introduced ot the abdomen over the next ten to fifteen minutes.[1] The total volume is referred to as a dwell[2] while the
fluid itself is referred to as dialysate. The dwell can be as much as 2.5 litres, and medication can also be added to the fluid immediately before infusion.[1] The dwell remains in the abdomen and waste
products diffuse across the peritoneum from the underlying blood vessels. After a variable period of time depending on the treatment (usually 4-6 hours[1]), the fluid is removed and replaced with fresh
fluid. This can occur automatically while the patient is sleeping (automated peritoneal dialysis, APD), or during the day by keeping two litres of fluid in the abdomen at all times, exchanging the fluids
four to six times per day (continuous ambulatory peritoneal dialysis, CAPD).[2][3]
The fluid used typically contains sodium, chloride, lactate or bicarbonate and a high percentage of glucose to ensure hyperosmolarity.
Complications
The volume of dialysate removed and weight of the patient are normally monitored; if more than 500ml of fluid are retained or a litre of fluid is lost across three consecutive treatments, the patient's
physician is generally notified. Excessive loss of fluid can result in hypovolemic shock or hypotension while excessive fluid retention can result in hypertension and edema. Also monitored is the color
of the fluid removed: normally it is pink-tinged for the initial four cycles and clear or pale yellow afterwards. The presence of pink or bloody effluent suggests bleeding inside the abdomen while feces
indicates a perforated bowel while cloudy fluid suggests infection. The patient may also experience pain or discomfort if the dialysate is too acidic, too cold or introduced too quickly, while difuse pain
with cloudy discharge may indicate an infection. Severe pain in the rectum or perinium can be the result of an improperly placed catheter. The dwell can also increase pressure on the diaphragm to
impair breathing, and constipation can interfere with the ability of fluid to flow through the catheter.[1]
TENCKHOFF CATHETER - allows permanent access to the peritoneal cavity. One end of the Tenckhoff catheter remains in the peritoneal cavity and the other extends outside of the body by about
four inches. The end outside of the body allows the dialysis fluid to be put inside of the tube and is sealed off when fluid is not being pumped into the catheter. Peritoneal dialysis is for use with longterm dialysis and may be performed at home by the patient himself. This allows the patient to continue dialysis without making frequent visits to the dialysis clinic.
A Tenckhoff catheter may be placed in the body using a local anesthetic. Most patients say that the procedure is more uncomfortable than painful. A physician may also insert the Tenckhoff catheter
during a minor surgical procedure requiring a general anesthetic. In either option, the affected area must heal for at least two weeks before the catheter can be used.

METABOLIC ACIDOSIS
>
>

is a disturbance in the body's acid-base balance that results in excessive acidity of the blood
is a pH imbalance in which the body has accumulated too much acid and does not have enough bicarbonate to effectively neutralize the effects of the acid.

Causes:

o
o
o

o
o
o

o
o

Inability to excrete the dietary H+ load

Renal failure - Diminished NH4 + production
Hypoaldosteronism - Type 4 RTA
Diminished H+ secretion - Type 1 (distal) RTA
Increased H+ load
Lactic acidosis - Numerous causes, including circulatory failure, drugs and toxins, and hereditary causes (see Lactic Acidosis)
Ketoacidosis - Diabetes, alcoholism, and starvation
Ingestions -Salicylates, methanol, ethylene glycol, isoniazid, iron, paraldehyde, sulfur, toluene, ammonium chloride, phenformin/metformin, and hyperalimentation fluids
GI HCO3 - loss
Diarrhea
Pancreatic, biliary, or intestinal fistulas

o
o

Ureterosigmoidostomy
Cholestyramine
Renal HCO3 - loss - Type 2 (proximal) RTA

Diagnosis:

Arterial blood gas sampling is essential for the diagnosis. The pH is low (under 7.35) and the bicarbonate levels are decreased (<24 mmol/l). Due to respiratory compensation
(hyperventilation), carbon dioxide is decreased and conversely oxygen is increased. An ECG can be useful to anticipate cardiac complications.

Other tests that are relevant in this context are electrolytes (including chloride), glucose, renal function and a full blood count. Urinalysis can reveal acidity (salicylate poisoning) or alkalinity
(renal tubular acidosis type I). In addition, it can show ketones in ketoacidosis.
Signs & Symptoms:
>
chest pain
> palpitations
> headache
> anxiety due to hypoxia
> decreased visual acuity
> nausea and vomiting
> weight loss
> muscle weakness and bone pains
> rapid breathing
Treatment:
Treatment is aimed at the underlying condition
Intravenous Bicarbonate is given at 50-100 mmol
Dialysis
Possible Complications:
>
Extreme metabolic acidosis can lead to neurologic and cardiac complications
>
Neurological: lethargy, coma, seizures.
>
Cardiac: arrhythmias (ventricular tachycardia), decreased response to epinephrine; both lead to hypotension (low blood pressure).
>
When very severe, metabolic acidosis may lead to shock or death

ASPIRATION PNEUMONIA
Aspiration pneumonia is a condition wherein there is inflammation of the lungs and airways to the lungs (bronchial tubes) from breathing in foreign material like foods, liquids, vomit, or fluids from
the mouth into the lungs
Causes:

Incompetent swallowing mechanism

Stroke
Patient is under general anesthesia / sedatives
Medications altering alertness
Decreased or absent gag reflex


Old age
Signs & Symptoms:
> Bluish discoloration of the skin caused by lack of oxygen
> Chest pain
> Cough with foul smelling sputum, with sputum containing blood and green sputum
> Fatigue
> Fever
> Shortness of breath
> Rapid breathing
> Wheezing
> Rapid pulse
> Difficulty in swallowing

Diagnosis:
A physical examination may reveal crackling sounds in the lungs and a rapid pulse.
The following tests may also help diagnose this condition:
Arterial blood gas
Bronchoscopy
Chest x-ray
CT scan of the chest
Sputum culture
Swallowing studies
Treatment:
Some people may need to be hospitalized. Treatment depends on the severity of the pneumonia. Patient with aspiration pneumonia will be given antibiotics, which treat bacteria and will be given
oxygen.
Complications:
> Spread of infection to the blood stream (bacteremia)
> Spread of infection to other areas of the body
> Low blood pressure
> Shock
> When severe, it can lead to death
Nursing responsibilities:
> Make sure the patient's bed is positioned or elevated to the proper angle
> Monitor the patient during feedings to ensure he or she doesnt choke
> Make sure that the patient receives the right food (food that is easy to swallow, digest, and wont further irritate the condition)

CARDIOPULMONARY ARREST
A cardiac arrest, also known as cardiopulmonary arrest or circulatory arrest, is the abrupt cessation of normal circulation of the blood due to failure of the heart to contract effectively during systole.

Cardiac arrest occurs when the heart is unable to maintain blood flow to the carotid artery sufficient to detect a pulse. The three most common conditions that lead to cardiac arrest are:

ventricular fibrillation - uncoordinated contraction of the cardiac muscle of the ventricles in the heart,

ventricular tachycardia - ventricles beat abnormally fast thus resulting to a pulse rate of more than 100 beats per minute, with at least three irregular heartbeats in a row.

asystole - a state of no cardiac electrical activity, hence no contractions of the myocardium and no cardiac output or blood flow.
Victims of cardiac arrest do not have enough circulation to maintain blood flow to the brain. Irreversible brain damage and death will usually occur within four minutes of the onset of cardiac arrest..
It is usually the result of a cardiac dysrhythmia. This arrest may be the result of primary cardiac disease or diseases which affect other organs.
A cardiac arrest is different from (but may be caused by) a heart attack or myocardial infarction, where blood flow to the still-beating heart is interrupted.
Risk Factors:
Predisposing causes of cardiopulmonary arrest include the following:
1) cellular hypoxia - a pathological condition in which the cells of the body is deprived of adequate oxygen supply.
2) vagal stimulation - Vagal stimulation slows the heart beat, and excessive stimulation can stop it entirely.
3) acid-base and electrolyte abnormalities
4) anesthetic agents - drug that brings about a state of anesthesia (state of absence of sensation)
5) trauma
6) systemic and metabolic diseases
Others include:
smoking
high blood pressure
high blood cholesterol
diabetes
being overweight or obese
physical inactivity
CAUSES:
"Hs and Ts"

Hypovolemia - A lack of circulating body fluids, principally blood volume. This is usually (though not exclusively) caused by some form of bleeding, anaphylaxis, or pregnancy with gravid
uterus.

Hypoxia - A lack of oxygen delivery to the heart, brain and other vital organs.

Hydrogen ions (Acidosis) - An abnormal pH in the body as a result of lactic acidosis which occurs in prolonged hypoxia and in severe infection, diabetic ketoacidosis, renal failure causing
uremia, or ingestion of toxic agents or overdose of pharmacological agents, such as aspirin and other salicylates, ethanol, ethylene glycol and other alcohols, tricyclic antidepressants, isoniazid,
or iron sulfate.

Hyperkalemia or Hypokalemia - excess and inadequate potassium can be life-threatening.

Hypothermia - A low core body temperature, defined clinically as a temperature of less than 35 degrees Celsius

Hypoglycemia or Hyperglycemia - Low blood glucose from overdose of oral hypoglycemics such as sulfonylureas, or overdose of insulin.

Tablets or Toxins - Tricyclic antidepressants, phenothiazines, beta blockers, calcium channel blockers, cocaine, digoxin, aspirin, acetominophen because these either results to hyperactivity
of the heart or suppression.

Cardiac Tamponade - Blood or other fluids building up in the pericardium can put pressure on the heart so that it is not able to beat.

Tension pneumothorax - The build-up of air into one of the pleural cavities, which causes a mediastinal shift. When this happens, the great vessels (particularly the superior vena cava)
become kinked, which limits blood return to the heart.

Thrombosis (Myocardial infarction)

Thromboembolism (Pulmonary embolism)

SIGNS AND SYMPTOMS:

Changes in the respiratory rate, depth, or pattern; a weak or irregular pulse; bradycardia; hypotension; unexplained changes in the depth of anesthesia; cyanosis; and hypothermia.
DIAGNOSTIC TEST:
The main diagnostic criterion to diagnose a cardiac arrest is lack of circulation, however there are a number of ways of determining this so in many cases, lack of carotid pulse is the gold standard for
diagnosing cardiac arrest.
Treatment:
Cardiopulmonary resuscitation (CPR) helping the heart and lungs function manually. CPR has three phases:
Basic Life Support:
A -- Establishment of an Airway.
B -- Breathing support.
C -- Circulation support.
Advanced Life Support:
D -- Diagnosis and Drugs.
E -- Electrocardiography.
F -- Fibrillation control.
Prolonged Life Support:
G -- Gauging a patient's response.
H -- Hopeful measures for the brain
I -- Intensive care.
Defibrillations - process in which an electronic device gives an electric shock to the heart to help reestablish normal contraction rhythms in a heart having dangerous arrhythmia or cardiac
arrest.

CLIENT IN CONTEXT

PRESENT STATE

INTERVENTIONS

EVALUATION

Informant: mother
Patient R.G., 11 years old, male, Roman
Catholic, born on July 1, 1998, from Ticad,
Bantayan Island, Cebu, was admitted for the first
time at Cebu Velez General Hospital on
September 30, 2009 via ambulance from Chong
Hua Hospital, accompanied by mother and
grandmother for complaints of difficulty breathing
noted about 1 month PTA and recurred 2 days
PTA. Patient was admitted under the services of
Dr. Monina Christina Cabral of the Department of
Pediatrics with a case number of 06750 and a
hospital number of 082047.
HISTORY OF PRESENT ILLNESS:
* renal failure and dyspnea
2 months PTA, the patient, after eating
enough bread, suddenly vomited and excreted a
small amount of loose, yellowish stool. Patient
was then noted by mother to have loss of appetite.
He did not eat lunch that day and refused to drink
water. He was noted to be very pale. Patient was
then brought to a nearby clinic and was examined
by a private doctor: Dr. Tecaro, a general
practitioner. He was prescribed with Oresol and
amoxicillin syrup 5 ml TID. Patient took Amoxicillin
only once and refused to drink the ORS
preparation or any other fluid despite constant
pleading of mother. The next day, patient still
refused to drink any fluid. Loss of appetite was still
noted. Mother also noticed that patient had no
urine output for almost 1 day. He was then
brought to the Bantayan District Hospital where
patient was administered furosemide with
unrecalled dose. No intravenous fluids were given.
Symptoms persisted so patients mother was
advised by the attending physician(unrecalled) to
transfer to a much equipped hospital.
Patient was then transferred to Chong
Hua Hospital and admitted under the
services of Dr. Cabral. He was taken
Serum Sodium, Serum Potassium and
Serum Creatinine levels upon admission

PHYSICAL EXAMINATION
Date Performed: October 1, 2009
General Appearance: Examined patient lying
on
bed,
awake,
responsive,
afebrile,
tachypneic and dyspneic with IVF on his bottle
2 PNSS 1L at 10 gtts/min infusing well at left
hand with O2 inhalation at 2L/min via nasal
cannula with pulse oximeter on left thumb with
ISA at right hand with clean, dry and intact
dressing on umbilical area with the following
V/S: BP= 120/100 mmHg, PR= 131 bpm, RR=
64 cpm, T= 38.0C/axilla.
Skin: rough skin with dark pigmentations on
hands and feet, non-pitting bipedal edema,
warm to touch, pinches easily and immediately
returns to its original position
Lymph Nodes: non-palpable
Head: normocephalic, symmetrical, HC = 53
cm, natural black hair, evenly distributed, scalp
is clean and dry with sparse dandruff visible,
head is hard and smooth without lesions,
round, erect and in midline, no abnormal facial
movements noted
Neck: (+) JVD, symmetric with head centered,
lymph nodes non palpable
Eyes: anicteric sclera, pale palpebral
conjunctivae, (-) PERRLA, (-) cardinal gaze,
black pigment on both upper eyelids, no
discharges, iris is round and uniform in color
Ears: pinna in line with outer canthus of eyes,
same color with facial skin, no aural
discharges, external ear is smooth without
lesions, lumps or nodules, small amount of
moist, yellow, odorless cerum noted
Nose: no nasal discharges, no lesions, color
consistent with the rest of the face, smooth,
symmetric, clear frontal sinuses
Mouth and Throat: dry and cracked lips, pale
oral mucosa, tongue at midline
Chest and Lungs: crackles heard on all lung
fields, use of accessory muscles and nasal
flaring during respiration
Heart: no heart murmurs, distinct S1 and S2,
tachycardic, (+) JVD, CRT= slightly pale

DRUG STUDY
Cefepime (Cepimax)
Classification: 4th generation cephalosporin
Mechanism of Action: Inhibits bacterial cell wall synthesis by binding to one or more of the penicillin-binding proteins (PBPs) which in turn inhibits the final transpeptidation step of peptidoglycan
synthesis in bacterial cell walls, thus inhibiting cell wall biosynthesis. Bacteria eventually lyse due to ongoing activity of cell wall autolytic enzymes (autolysis and murein hydrolases) while cell wall
assembly is arrested.
Indication: Treatment of uncomplicated and complicated urinary tract infections, including pyelonephritis caused by typical urinary tract pathogens; monotherapy for febrile neutropenia; uncomplicated
skin and skin structure infections caused by Streptococcus pyogenes; moderate to severe pneumonia caused by pneumococcus, Pseudomonas aeruginosa, and other gram-negative organisms;
complicated intra-abdominal infections (in combination with metronidazole). Also active against methicillin-susceptible staphylococci, Enterobacter sp, and many other gram-negative bacilli.
Contraindication: Hypersensitivity to cefepime, other cephalosporins and penicillins, pregnancy, lactation, cautiously used with patients having liver and renal diseases
Adverse Effects: Fever, headache, rash, pruritus, diarrhea, nausea, vomiting, pain, erythema at injection site, anaphylaxis, coma, encephalopathy, leukopenia, neutropenia, hallucinations, myoclonus,
thrombocytopenia
Nursing Considerations:

Obtain specimen for culture and sensitivity prior to the first dose; monitor for signs of anaphylaxis during first dose

Inform prescriber of all prescriptions, OTC medications, or herbal products you are taking, and any allergies you have. Do not take any new medication during therapy unless approved by
prescriber.

Report immediately any redness, swelling, burning, or pain at injection/infusion site; itching or hives; difficulty swallowing or breathing.

Maintain adequate hydration (2-3 L/day of fluids unless instructed to restrict fluid intake).

Inform patient or SO of the possible side effects of the drug

Salbutamol
Classification: beta 2 adrenergic receptor antagonist
Mechanism of Action: stimulates beta(2)-adrenergic receptors. Binding of albuterol to beta(2)-receptors in the lungs results in relaxation of bronchial smooth muscles. It is believed that salbutamol
increases cAMP production by activating adenylate cyclase, and the actions of salbutamol are mediated by cAMP. Increased intracellular cyclic AMP increases the activity of cAMP-dependent protein
kinase A, which inhibits the phosphorylation of myosin and lowers intracellular calcium concentrations. A lowered intracellular calcium concentration leads to a smooth muscle relaxation. Increased
intracellular cyclic AMP concentrations also cause an inhibition of the release of mediators from mast cells in the airways.
Indications: Acute asthma, symptom relief during maintenance therapy of asthma and other conditions with reversible airways obstruction (including COPD and bronchitis), protection against
exercise-induced asthma, can be aerosolized with a nebulizer for patients with cystic fibrosis, along with ipratropium bromide, acetylcysteine, and pulmozyme.
Contraindication: hypersensensitivity to drug, ischemic heart disease, cardiac arrhythmias
Adverse Effects: The most common side effects are of fine tremor, nervousness, headache, muscle cramps, dry mouth, and palpitation. Other symptoms may be tachycardia (rapid heart rate),
arrhythmias, flushing, myocardial ischaemia, and disturbances of sleep and behaviour.Rarely occurring, but of importance, are allergic reactions of paradoxical bronchospasm, urticaria, angioedema,
hypotension, and collapse, whilst high doses may cause hypokalaemia (low potassium levels), especially in patients with renal failure.
Nursing Considerations:

Use this medication as directed. Do not increase your dose or use this more frequently than directed. Excessive use may lead to a loss of effectiveness while increasing the chance for side
effects.

Do not stop using this medication without first consulting your doctor. If symptoms do not improve or worsen after using this drug or if you find yourself using this more than usual, contact
your doctor immediately.

If this medication appears to be losing its effectiveness, notify your doctor. A change in your therapy may be necessary.

Use cautiously in patients with cardiovascular disorders.

Warn the patient about the risk of paradoxical bronchospasm and if it occurs, stop drug immediately.
Famotidine
Classification: H2-receptor agonist

Mechanism of Action: A potent competitive inhibitor of histamine at histamine receptor sites at gastric parietal cells. Inhibits basal, nocturnal, meal-stimulated and pentagastrin- stimulated gastric
secretions; also inhibits pepsin secretion.
Inidication: For short term of active duodenal ulcer, maintenance therapy for duodenal ulcer patients on reduced dosage after healing of active ulcer. For treatment of pathologic hypersecretory
conditions, benign gastric ulcer, gastroesophageal reflux disease, gastritis.
Contraindication: Hypersensitivity to drug, pregnancy, cautiously use to patients with renal or hepatic diseases
Adverse Effect: Increase in BUN and Serum Creatinine, Thrombocytopenia, Rash, acne, pruritus, dry skin, flushing, Constipation, diarrhea, Dizziness, headache, confusion, depression
Nursing Consideration:

Pain relief may not be experienced for several days after starting therapy

Take an hour before a meal

Not to take with other acid-reducing products

Decrease dose with renal failure