Transudate

April 29, 2012   Dr. Joe Steve   No comments

Edema is excessive accumulation of fluid in the extravascular spaces. Edema fluid can accumulate in the interstitial space and body cavities. Edema can be divided in to 2 types:

  • Exudate (Exudatory edema)
  • Transudate (Transudatory edema)

Exudate (Exudatory edema)
Exudatory edema occurs with acute inflammation. Here increased vascular permeability will allow excessive leakage of plasma protein containing fluid into the extravascular compartment. This edema fluid contains high plasma proteins, fibrin and neutrophils. Therefore exudate will appear turbid or opaque.

Transudate (Transudatory edema)
Transudate occurs with normal vascular permeability, in the absence of inflammation. Since vascular permeability is normal there will be no excessive plasma protein leakage. Therefore transudate will have low protein level and due to absence of fibrin and inflammatory cells it will appear clear and transparent.

Transudate vs Exudate

  • Appearance of the exudate is turbid/opaque and that of transudate is clear and transparent.
  • Exudate contains high level of protein(more than 30g/dl) and transudate contains low level of proteins(less than 30g/dl).
  • Specific gravity of exudate is more than 1.020 and that of transudate is less than 1.012
  • Exudate will contain fibrin but transudate will not have fibrin.
  • There are lot of inflammatory cells(mainly neutrophils) can be seen in exudate but transudate will have few or no inflammatory cells.

The mechanism of formation of transudate
Starling forces
Starling forces(hydrostatic and oncotic pressure) describe the forces that control fluid movement across the capillary wall in normal health.

Hydrostatic pressure pushes fluid out of the blood vessel across the capillary wall, while colloid osmotic pressure(oncotic pressure) pulls fluid into the vessel. Hydrostatic pressure depends on the blood pressure driven by the heart, while colloid osmotic pressure depends on the number of large undissolved particles in the plasma, mainly plasma proteins.

Hydrostatic pressure high at the arteriolar end and drops along the capillary and lowest at the venous end of the capillary but the oncotic pressure remains the same. Therefore net fluid movement at the arteriolar end of the capillary is outwards and at the venular end is inwards. This is how fluid movement between capillaries and tissue occur in normal health. Any excess fluid left behind will be cleared by lymphatics. Alteration of these forces results in formation of transudate.

Causes of transudate formation
Factors that would cause excessive outward movement of fluid across the capillary wall will contribute to formation of transudate.

  • Increased hydrostatic pressure
  • Reduced oncotic pressure
  • Lymphatic obstruction – Lymphedema

An important point to remember is generalized edema always transudatory.

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Postpartum Exercise

April 28, 2012   Dr. Joe Steve   No comments

Postpartum exercise is useful to teach the mother simple exercises designed specially for the muscles of her pelvic floor and abdominal wall during the puerperium(the period following childbirth). Postpartum exercises may be started the day after delivery, and the mother should be instructed to continue postpartum exercises at home for at least three months. Exercises after pregnancy helps to strengthen muscles, which have stretched during pregnancy and labour, and to re-educate a correct posture and thus help to prevent backache.

STEP 1
Lie on the back with the body and legs straight,i.e on supine position. Breathe in slowly, expanding chest. Pull the abdominal muscles in and press the lower part of the back to the floor. Repeat this step for 5 to 10 times.

STEP 2
Lie on supine position. Then raise the head from the floor, bringing it close to the chest. Repeat this step for 5 to 10 times.

STEP 3
Lie on supine position. Put the arms straight out at sides, then raise them over the head until hands meet. Keeping the arms stiff, lower they rest at the side. Repeat this step for 5 to 10 times.

STEP 4
Lie on supine position. Then bring one leg up over the body until the foot touches the buttocks.Straighten and lower it, then repeat the exercises with the other leg. Repeat this step for few times.

STEP 5
Lie on the back with the knees partially bent. With arms straight out, raise your body to a 45 degrees angle. Later, when you are stronger perform the exercises with hands clasped behind the head. Repeat this step for few times.

STEP 6
Without using the hands raise one leg at a right angle to the body. Then do the same with other leg. Later when you are strong raise both legs at once. Repeat this step for 5 to 10 times.

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Treatment of Oleander Poisoning

April 21, 2012   Dr. Joe Steve   No comments

Thevetia peruviana and Nerium oleander are poisonous plants. All parts of these plants are poisonous due to the presence of cardiac glycosides. Poisoning mostly occurs due to deliberate ingestion of seeds.

Clinical features of Oleander Poisoning

  • Nausea and vomiting. Vomiting 6-12 hours after the ingestion implies significant absorption of toxin.
  • Bradycardia, variable heart block, hypotension, ventricular arrhythmias.
  • Convulsions and coma.
  • Hyperkalaemia.
  • Xanthopsia.

Investigations of Oleander Poisoning

  • ECG with rhythm strip
  • Serum electrolytes

Treatment of Oleander Poisoning

  • Even asymptomatic patients should be observed for at least 24 hours.
  • Continuous monitoring of cardiac rhythm. If facilities for cardiac monitoring are not available, perform frequent electrocardiograms.
  • Maintain fluid balance chart.
  • Perform gastric lavage if seen within 2 hours of ingestion.
  • Give activated charcoal. Activated charcoal is a useful adsorbent of many poisons if given within one hour, provided at least 10 times the volume of the poison is given. Suspend 50g in 200ml of water. Recommended dose is 1g/kg.
  • Repeat estimation of serum Potassium 4 hourly to detect hyperkalaemia.
  • If serum Potassium is above 5.5mmol/l, consider antidigoxin antibody therapy and seek specialist opinion.
  • Give normal saline with added KCl 40mmol or 20ml of 15% KCl if serum Potassium is below 3mmol/l.
  • Treat convulsions with Diazepam 5-10mg intravenously.
  • For bradycardia of less than 40 beats per minute or second degree AV block give a bolus dose of Atropine 0.6-1.2mg intravenously or an infusion of 6mg of Atropine in 500ml of normal saline. Titrate to maintain heart rate between 60 and 90 beats per minute.

Caution: Tachycardia and Atropine poisoning.

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Fat Necrosis

April 15, 2012   Dr. Joe Steve   No comments

What is fat necrosis
Fat necrosis is the necrosis of adipose tissue/fat cells due to action of lipase enzymes. Fat necrosis gives rise to special morphological appearance due to release of triglycerides and fatty acids from damaged adipose tissue.
Types of fat necrosis
According to the causative agents fat necrosis can be divide into two types:

  • Enzymatic fat necrosis – Caused by enzymes especially pancreatic enzymes.
  • Nonenzymatic fat necrosis/Traumatic fat necrosis – Commonly due to trauma to tissues with high fat content.

Enzymatic fat necrosis
This is most commonly seen in acute pancreatitis and other forms of acute pancreatic injury. Damaged pancreatic acinar cells release lipase enzymes into the surrounding tissues and damaged the adipose tissue. Lipase enzymes breakdown triglycerides in the adipose tissue to form free fatty acids. Fatty acids combined with Calcium and form insoluble salts (fat saponification). These get deposited as chalky white masses in the peritoneal cavity.

Nonenzymatic fat necrosis/Traumatic fat necrosis
This is commonly due to trauma(therefore it is also called traumatic fat necrosis) to the tissues with high fat content such as breast, subcutaneous tissue (especially in obese people and babies after traumatic delivery). Disrupted adipose tissue releases triglycerides and lipase enzymes into the surrounding tissues. Triglycerides induce a granulomatous inflammatory response in the surrounding tissues. Furthermore, released lipases get activated and breakdown triglycerides into free fatty acids.

Symptoms and signs of fat necrosis
These lesions are felt as hard irregular nodules due to fibrosis and calcium deposits. In breast these lesions closely mimic carcinoma in clinical examination and mammography (due to calcification). Fine needle aspiration and/or excision biopsy of the lesion is necessary for diagnosis.

Histology of fat necrosis
Histological picture is characterized by presence of many lipid ingested foamy cells, Touton’s giant cells, vague granulomata composed of foamy cells and epithelioid cells, Calcium deposits and lipid pools. Fibrosis is seen in older lesions. In enzymatic fat necrosis histology is similar to nonenzymatic fat necrosis, except that granulomatous nature and Touton’s giant cells are not prominent as in enzymatic fat necrosis.

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Testicular Feminization Syndrome/Androgen insensitivity syndrome

April 02, 2012   Dr. Joe Steve   No comments

Testicular feminization syndrome is another important type of intersex. The affected individuals have the male genotype of XY, but the external appearance is female due to resistant to androgen hormones. Testicular feminization syndrome has two types:

  • Complete testicular feminization syndrome
  • Incomplete testicular feminization syndrome

In complete testicular feminization syndrome there is failure to develop penis and other male body parts. Complete form occurs in as many as 1 in 20,000 live births. The degree of sexual ambiguity varied widely with incomplete form.

Causes of testicular feminization syndrome
Testicular feminization syndrome is due to various genetic abnormalities in the X chromosome which make the body unable to react to androgen hormones that responsible for the male phenotype. The male gonads are present and start the normal production of testosterone hormone from fetal life. But due to on or more of the following reasons, the testosterone fails to bring about the normal male appearance of the fetus, resulting in a female phenotype.

  • The absence of the specific receptors for the binding of testosterone at cellular level.
  • Absence of the cellular enzymes responsible for the conversion of testosterone to its active form, dihydrotestosterone.
  • This leads to production of oestrogen and breast enlargement.

Symptoms and signs of testicular feminization syndrome

  • The external appearance is female
  • The skin is smooth, with very little body hair and the axillary/pubic hair is also sparse.
  • The body contours all resemble female with well-formed breasts.
  • Most of the cases the vulva is normal in appearance with a normal looking vagina, but when examined properly the vagina is short and blind ended. Therefore the individual can have normal sexual intercourse but has no capacity to conceive, i.e they are infertile.
  • Some individuals will have partially closed vaginal lips.
  • Enlarged clitoris.
  • There is no uterus or fallopian tubes. Hence they often present during the adolescence with primary amenorrhoea.
  • Testes may be present either in the perineal region, inguinal region(may present as inguinal hernia) or intra abdominally. These internal testes must be removed surgically as they carry an increased risk of malignant transformation( into dysgerminoma in 5% of cases).

Investigations of testicular feminization syndrome

  • Ultrasound scan of the pelvis
  • Blood test to detect testosterone, follicle stimulating hormone(FSH) and luteinizing hormon levels.
  • Karyotyping

Complications of testicular feminization syndrome

  • Testicular cancers
  • Infertility
  • Psychological and social problems

Treatment of testicular feminization syndrome

  • Surgical removal of inguinal or intra abdominal testicular tissue ideally before puberty as they carry a high risk of testicular cancer.
  • Oestrogen replacement therapy.
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Pelvic Pain

March 31, 2012   Dr. Joe Steve   No comments

Pelvic pain is a symptom experienced by every female at lease once in her lifetime. Pelvic pain does not always indicate an organ disease. When it is of organic origin it can be either due to pathology in the female reproductive organs or other pelvic viscera such as the bladder and the rectum. Pelvic pain can be classified as acute pain and chronic pain depending on the duration from its onset.

Acute pelvic pain
This is a common presentation in gynecological casualty. If the pain is originating from the reproductive tract, the aetiology could be one or more of the followings.

Causes for acute pelvic pain

1. Disturbed pregnancy

  • Abortion/Miscarriage
  • Hydatidiform mole
  • Ectopic pregnancy

2. Haemoperitoneum

  • Ruptured ectopic pregnancy
  • Ruptured corpus luteum cyst or follicular cyst
  • Following uterine perforation (Dilatation and curettage, Termination of pregnancy, Insertion of IUCD)

3. Pelvic endometriosis

4. Torsion of an ovarian cyst/Haemorrhage in to a cyst

5. Red degeneration of fibroid

6. Pelvic infections

7. Pelvic adhesion following inflammation or surgery, uterine prolapse and rarely tumors of the reproductive tract

8. Infection of the other pelvic viscera such as appendicitis, urinary tract infections and neoplasms

Diagnosis of the exact cause for pelvic pain
A careful history, examination followed by investigations can most of the time identify the pathology, so that specific treatment can be done. Onset, nature, severity and localization of the pelvic pain, presence of any associated symptoms such as vomiting, fever, vaginal discharge, past history of intervention and surgeries in the pelvis are important points to note in the history. General physical examination to detect complications such as shock due to internal bleeding and sepsis following infection should be given priority, especially in cases of acute pelvic pain. Detection of pelvic lumps, localized areas of tenderness, vaginal discharge and tenderness on vaginal examination are positive signs. If the pathology is suggestive of large bowel in origin, per rectal examination is also necessary. Initial resuscitation should be started in cases of dehydration, shock and sepsis irrespective of the aetiology and investigations should be done simultaneously to obtain a definitive diagnosis.

Investigations in pelvic pain

  • Full blood count and ESR – To detect any infections.
  • Urine full report and if indicated culture.
  • Urine pregnancy test – If the history is suggestive, to consider the possibility of pregnancy and associated complications.
  • Ultra sound scan – This is helpful in identifying the pathology as well as in differentiating gynecological from non-gynecological aetiologies.
  • Laparoscopy – In the event of doubtful diagnosis, laparoscopy is a very useful technique, which aids in obtaining a definitive diagnosis as well as implementing immediate therapeutic measures.

Treatments of pelvic pain
Pain relief is important with the usage of analgesics. Narcotic analgesics are withheld in the initial period if the continuous supervision for the development of complications is necessary. If the diagnosis is suggestive of a non-gynecological cause, the patient should be transferred to a respective specialty following basic resuscitation. Specific treatment varies with the pathology identified.

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Intravenous Anaesthetic Agents

March 29, 2012   Dr. Joe Steve   No comments

Intravenous anaesthetic agents are used to induce anaesthesia, as induction is more rapid and smoother than with inhalational agents. The ideal intravenous anaesthetic agents must produce rapid onset of action and rapid recovery with minimal cardiovascular and respiratory depression. Non of the currently available agents meet ideal requirements. Following are the commonly used intravenous anaesthetic agents.

Thiopentone Sodium

  • Thiopentone Sodium is the most commonly used intravenous anaesthetic agent.
  • It is a barbiturate and is administered as a 2.5% solution(25mg/ml) in a dose of 4mg/kg.
  • Intravenous injection produces anaesthesia in less than 30 seconds(arm-brain circulation time) and regain consciousness within 5-10 minutes.
  • Does not provide analgesia.
  • Depressed the myocardium and produces peripheral vasodilatation.
  • Depresses respiration. Apnoea may occur. May precipitate laryngeal and bronchial spasm.
  • Immediate recovery depends on the redistribution of the agent in the body. After recovery of consciousness the redistributed drug is metabolized in the liver and excreted via urine. Metabolism and elimination can take up to 24 hours,so its use should be avoided in outpatients.
  • Intra arterial injections can cause spasm and thrombosis which may precipitate ischemia and gangrene.
  • Perivenous injections can cause tissue necrosis.
  • Allergic reactions may occur.
  • Thiopentone Sodium is contraindicated in porphyria and bronchial asthma.

Methohexitone Sodium

  • It is a barbiturate.
  • Administered in a dose of 1mg/kg of 1% solution(10mg/ml).
  • Recovery is faster than thiopentone. Hangover effect is less. Therefore it is useful when rapid recovery is required.
  • Cardiovascular and respiratory depression is less than that with thiopentone.
  • Tremors, hiccup and pain on injection.

Propofol(Diprivan)

  • It is a nonbarbiturate.
  • A dose of 2-2.5mg/kg is required.
  • Recovery is very rapid with little hangover effect.
  • Blood pressure drops due to vasodilatation.
  • Apnoea may occur. No bronchospasm is seen.
  • Pain on injection. Allergic reactions may occur.

Etomidate

  • A dose of 0.3mg/kg is used to produce anaesthesia.
  • Cortisol synthesis is suppressed.
  • Involuntary movements and pain on injection are common.

Ketamine

  • Is a phencyclidine derivative.
  • Produces dissociative anaesthesia rather than generalized depression of the central nervous system. Produces anaesthesia within 30-60 seconds. Produces analgesia with a dissociation of the patient from his surroundings.
  • IV dose of 1-2mg/kg produces anaesthesia for 10-15 minutes. Additional doses can be used every 10 minutes to prolong anaesthesia. Can be given intramuscular in a dose of 10mg/kg. Available in 10mg/ml and 50mg/ml solutions.
  • It’s a potent analgesic.
  • Blood pressure, heart rate, intracranial pressure and intraocular pressure will be increased. Therefore avoid in hypertension, ischemic heart disease, head injury and open eye surgery.
  • Useful in the shock patients.
  • Muscle tone is maintained, therefore airway obstruction doesn’t occur.
  • Pharyngeal and laryngeal reflexes are preserved, but risk of aspiration exists.
  • Produces bronchodilatation, therefore useful in asthmatics.
  • Increase salivation may require Atropine.
  • Unpleasant dreams and hallucinations occur, the incidence of which can be reduced by concomitant administration of Diazepam.

Benzodiazepines(Diazepam,Midazolam)

  • Given IV to induce anaesthesia.
  • Has sedative, amnesia, anxiolytic and anticonvulsant effects. Produce muscle relaxation.
  • Large IV doses may produce cardiac and respiratory depression.
  • Diazepam given orally or IV (5-20mg)
  • Midazolam IV induction dose is 0.3mg/kg.

 

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Pelvic Inflammatory Disease (PID)

March 25, 2012   Dr. Joe Steve   No comments

What is pelvic inflammatory disease
Pelvic inflammatory disease is a general term for acute, sub acute, recurrent or chronic infection/inflammation of reproductive pelvic organs such as ovaries, uterus and fallopian tubes. This is usually leads to scar formation and adhesion to nearby tissues and organs. Clinical assessment of a patient with pelvic inflammatory disease includes identification of the affected organs, the stage of the infection and the causative agent.

Causes of pelvic inflammatory disease
It is commonly due to bacterial infections but viral, fungal and parasitic infections also cause PID.PID is most commonly seen in patients with sexually transmitted infections especially gonorrhea and chlamydia. Postpartum infections, abortion, intrauterine device related infections, lymphatic and hematogenous spread is also possible.

Symptoms of pelvic inflammatory disease

  • Lower abdominal pain
  • Fever
  • Offensive vaginal discharge
  • Lethargy, malaise
  • Anorexia and nausea
  • Dysuria and increased frequency
  • Painful intercourse (Dyspareunia)
  • Irregular menstrual bleeding

Signs of pelvic inflammatory disease
General signs

  • Ill looking
  • Increased body temperature
  • Increased pulse rate

Abdomen

  • Distended abdomen if complicated with paralytic ileus.
  • Tender and rigid if associated with peritonitis.
  • Localized inflammation can be detected by eliciting tenderness in specific areas. For example bilateral iliac fossa tenderness in salpingo oophoritis.
  • Pelvic examination demonstrates a purulent vaginal discharge . Inspection of the vagina and cervix with speculum shows inflammatory changes.Assessment of the size of the uterus and detection of adenexal masses and tenderness are also important.

Diagnosis of pelvic inflammatory disease
There is no precise test to diagnose pelvic inflammatory disease. Therefore the diagnosis basically depend on the symptoms, signs and investigations,so it is a clinical diagnosis. If the patient is having above symptoms and signs, a high vaginal swab should be taken and send for culture and ABST(Antibiotic Sensitivity Test) before starting any antibiotics. Blood culture may also be necessary in indicated cases. Full blood count and ESR will help the diagnosis. Ultrasound scan of the abdomen and pelvis will detect tubo ovarian masses(abscesses) and exclude other differential diagnosis.

Treatment of pelvic inflammatory disease
Acute pelvic infections
Treatment modality varies with the severity of the infection and associated complications. Mild cases can be treated in an out patient clinic with oral antibiotics to cover possible pathogens after specimens have been taken to identify the causative organisms. Most commonly used antibiotics are Metronodazole and Amoxycillin.
Severe infection has to be treated in a ward. The patient should be provided bed rest. Dehydration and acidosis have to be corrected by giving intravenous fluids. If there is abdominal distension or ileus, nesogastric suction may be necessary. Intravenous antibiotics must be administered initially till the disappearance of clinical features. Metronidazole, Ampicillin, Cephalosporin and Gentamicin are the most commonly used antibiotics. Antibiotics can be changed according to the result of ABST. Continuous monitoring of vital signs is necessary and exploratory laparotomy may have to be performed, if there is clinical suspicion of abscess rupture.

Chronic pelvic infection
Place of continuous antimicrobial treatment is controversial. If there is a causative agent like IUCD, it should be removed. Antibiotic treatment with Ampicillin, Cephalosporin and Tetracycline may be indicated for 3-4 weeks. Symptomatic relief should be achieved with analgesia.

Surgical treatment
Surgical treatment depends on the extent of the disease and the fertility requirement ofthe female.

  • Salpingostomy to evacuate a pyosalphinx.
  • Salpingo-oophorectomy to remove a tubo ovarian mass.
  • Total abdominal hysterectomy and bilateral salpingo-oophorectomy in severe cases.

Complications of pelvic inflammatory disease

  • Peritonitis(pelvic or generalized)
  • Adynamic ileus
  • Pelvic cellulitis with thrombophlebitis
  • Abscess formation
  • Adhesion
  • Infertility
  • Ectopic pregnancy
  • Hydrosalphinx, pyosalphinx and tubo ovarian masses
  • Chronic pelvic pain

 

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Acute Tubular Necrosis

March 05, 2012   Dr. Joe Steve   No comments

Acute tubular necrosis is acute suppression of renal functions associated with tubular epithelial injury. Acute tubular necrosis is due to

  • Ischemic injury
  • Toxic injury

Acute tubular necrosis due to ischemic injury
There is acute hypoperfusion due to hypotension. The hypoperfusion could be due to:

  • Acute loss of body fluids causing shock such as extensive haemorrhage following trauma, extensive burns and dehydration following severe diarrhoea.
  • Septic shock
  • Pancreatitis

Acute tubular necrosis due to toxic injury(nephrotoxins)
Toxic injury to the kidney could be due to nephrotoxins such as:

  • Organic solvents – carbon tetrachloride, ethylene gycol
  • Heavy metals – Mercury, Lead
  • Antibiotics – Amphotericin B, Gentamycin
  • Chemotherapeutic agents – Methotrxate, Cisplatin
  • Endogenous toxins – Myoglobin in severe skeletal muscle injury following extensive exercise, snake venom, extensive crush injury and haemoglobin in severe intravascular haemolysis.

Clinical features of acute tubular necrosis

  • Oliguria or anuria
  • Rapid increasing in serum creatinine levels
  • Urine analysis – degenerated epithelial cells and granular casts.

Macroscopic appearance of the kidney in acute tubular necrosis

  • Kidney is pale and swollen.
  • Cortex is pale and swollen, medulla is congested.

This is typically seen in acute tubular necrosis following shock.

Microscopic appearance of the kidney in acute tubular necrosis

  • Necrosis of tubular epithelial cells.
  • Tubular lumina contain desquamated necrotic epithelial cells.
  • Interstitial oedema and mononuclear inflammatory infiltration.

Once the insulting agent is removed the tubular epithelial regeneration occurs and complete resolution is possible.

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Pathology of Acute Pyelonephritis

March 01, 2012   Dr. Joe Steve   No comments

Pathology of acute pyelonephritis is a tubulointerstitial inflammation due to infectious causes. The infectious agent is commonly a bacterium which causes infection in the lower urinary tract(cystitis). Acute infection of the renal parenchyma with these organisms causes acute pyelonephritis and repeated infections can later lead to chronic pyelonephritis.
Route of bacterial entry:

  • Ascending infections from the lower urinary tract. This is the most common route. Commonly involved bacteria are those that cause urethritis and cystitis( usually derived from the normal fecal flora) are E. coli, Proteus, Klebsiella and Enterobactor.
  • Haematogenous spread usually following septicaemia.

The most important phenomenon which facilitate ascend of bacteria from the bladder to the kidney is vesicoureteral reflux. This could be due to incompetence of vesicoureteral valve, urinary tract obstruction or persistent bladder atony due to spinal cord injury. Intrarenal reflux propel bacteria into the renal pelvis and parenchyma.
Risk factors for acute pyelonephritis:

  • Urinary tract obstruction
  • Vesicoureteral reflux
  • Instrumentation of the urinary tract such as catheterization(facilitate ascend of lower urethral flora into the bladder).
  • Pregnancy(bacteriuria is relatively common during pregnancy)
  • Preexisting renal lesions
  • Diabetes mellitus
  • Immunodeficiency

 

Clinical features of acute pyelonephritis

  • Fever
  • Dysuria
  • Pain in the costovertibral angle on the affected area
  • Nausea and vomiting

 

Pathology of acute pyelonephritis
Bacteria enters the renal parenchyma and cause acute inflammation in the renal tubules and the interstitium and infection settles in the renal parenchyma. Acute inflammation leads to oedema in the interstitium and extravasation of neutrophils into the interstitium. Then these neutrophils invade the renal tubules cause tubulitis, tubular destruction and formation of microabscesses in the renal tubules. Infection gradually spreads through the entire renal parenchyma, usually sparing the glomeruli.
Macroscopic appearance of acute pyelonephritis
Surface of the kidney is dull and opaque. Small multiple subcapsular abscesses may be seen. Cut surface of the kidney will show multiple small abscesses or streaks of pus in the cortex. Features of complications may or may not be present.
Microscopic appearance of acute pyelonephritis
Interstitial oedema and neutrophil infiltration can be seen. Tubulitis and microabscesses in the renal tubules with the pus cell casts in the tubules can be seen under the microscopy.
Complications of acute pyelonephritis
In most patients with acute pyelonephritis follow an uncomplicated course with treatments. However patients with obstruction, diabetes mellitus and immunodeficiency can have complications of acute pyelonephritis.

  • Pyonephrosis, accumulation of purulent exudate in the kidney. This is usually due to associated complete or almost complete obstruction in the renal pelvis/ureters preventing drainage of the exudate.
  • Perinephric abscess. Extension of suppurative exudate through the renal capsule into the perinephric tissue.
  • Renal papillary necrosis.
  • Recurrent acute pyelonephritis may leads to chronic pyelonephritis.

 

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