HYDROCEPHALUS

CLASSIFICATION & PATHOPHYSIOLOGY

DR.SHIVASHANKAR.B.M .

Hydrocephalus
HYDROCEPHALUS term is derived from Greek word, Hydro-water and cephalous-head. It is a pathological condition rather than a specific disease. Is defined by as a disproportionate increase in the amount of CSF within The cranium,usually in association with a rise in ICP that result from impaired circulation and absorption of CSF or in the rare circumstances from increased production by a choriod plexus papilloma.

Affects both pediatric and adult age group patient. It has been estimated that 7,00,000 children and adults are living with hydrocephalus. Incidence in pediatric age group 1 in 500 live births hence making it one of the most common disabilities even more common than Down syndrome and Deafness. Also it is the leading cause of brain surgery for children. Pediatrics hydrocephalus may also be a heritable condition mainly affecting males.

Refrences have been found in ancient Egyptian medical literature from 2000 B.C.to 500A.D. First described by HIPPOCRATES in 4th century B.C. But more accurate description given by roman physician GALEN in 2nd century A.D. First clinical description and operative procedure for hydrocephalus appears in Al-Tasrif(1000A.D.)by Arab surgeon Abu-al-Qasim who clearly described the evacuation of superficial intracranial fluid in hydrocephalic children.

ANATOMY OF VENTRICULAR SYSTEM

 To understand the pathophysiology of HCP , its first necessary to understand the normal dynamics of CSF flow.  Ventricles are set of structures containing CSF in brain which is continuous with central canal of spinal cord. Composed of 4 ventricles: 2 Lateral ventricles Third ventricle Fourth ventricle

ANTERIOR HORN POSTERIOR HORN INTERVENTRICULAR FORAME THIRD VENTRICLE INFERIOR HORN CEREBRAL AQUEDUCT FOURTH VENTRICLE

SPINAL CANAL

It is produced mainly by ependymal cells of choroid plexus found in components of ventricular system except from cerebral aqueduct and occipetal and frontal horns of lateral ventricle Additional amounts of fluid are secreted by all the ependymal surfaces of the ventricles and the arachnoid membranes, and a small amount comes from the brain itself through the perivascular spaces that surround the blood vessels entering the brain.

Lateral ventricle Foramen of Monro 3rd ventricle Aqueduct of Sylvius 4rth ventricle

3 foramina Cisterns of sub arachnoid space

central canal of spinal cord

Lumbar cistern

Around cerebral cortex

CSF pathway

VOLUME PRODUCTION

150ml 20ml/hr(80% by choroid plexus) Arachnoid villi(pressure dependent) Reduced K and Ca ions Increased Cl and Mg ions pH=7.33 to 7.35

ABSORBTION

RELATIVE TO PLASMA

PRESSURE

5 to 15 mmHg(6 to 18cm of water)

1. PROTECTION- It acts as a shock absorber. 2. TRANSPORT-Act as a vehicle for delivering nutrients and removing waste. 3. It flows between the cranium and spine and compensates for changes in intra cranial blood volume.

The fluid then flows around the superior sagittal sinus. It reabsorbed via arachnoid villi into venous system. ARACHNOID GRANULATIONS-these are small protrusions of arachnoid which protrude into the venous sinuses of brain allows csf exit from brain and enter blood. The largest arachnoid granulation lies along the superior sagittal sinus. The arachnoid villi act as a one way valve.Normally PRESSURE OF CSF >PRESSURE OF VENOUS SYSTEM.So CSF is drained through villi into venous blood. Some amount of CSF is also drained through lymphatics assossiated with extra cranial nerves,ex.-through axons of olfactory nerve via cribriform plate.

1. COMMUNICATING HYDROCEPHALUS  Non-obstructive hydrocephalus  It is caused by impaired cerebrospinal fluid resorption due to obstruction of CSF flow outside the ventricular system,usually at the level of basal sub arachnoid cistern or at the arachnoid granulations. 2. NON COMMUNICATING HYDROCEPHALUS  Obstructive hydrocephalus  It is caused by a CSF-flow obstruction with in the ventricular system ultimately preventing CSF from flowing into the subarachnoid space (either due to external compression or intraventricular mass lesions). Both communicating and non communicating can be congenital or aquired.

NonNon-obstructive (communicating)
This type results from problems with the production or absorption of CSF. The most common is caused by bleeding into the subarachnoid space in the brain.

Communicating Hydrocephalus:
y There is free flow throughout the ventricular system. y Impaired CSF resorption by the arachnoid granulation accounts for majority of cases 1. SAH 2. Infectious meningitis 3. Malignant meningitis 4. Granulomatous mningitis : TB , sarcoidosis 5. Altered venous Dynamics : Vein of Galen malformation, venous obstruction

Non-Communicating Hydrocephalus (Intraventricular obstruction)

y Ventricular dilatation caused by intraventricular obstruction at or above the the outlet foramina of the 4th ventricle y Causes: 1. Lateral ventricle 2. Foramen of Monro 3. 3rd ventricle 4. Aqueduct of sylvius 5. 4th ventricle

Lateral Ventriclar causes:

1. Intrinsic tumor: ependymoma 2. Ventriculitis: due to intraventricular adhesions 3. Extraventricular Tumour: mass effect from large parenchymal mass

Ventriculitis case 1

Ventriculitis case 2

Neuroepithelial Cyst

Obstruction of Foramen of Monro:

1. Tumour : colloid cyst , subependymal giant cell astrocytoma 2. Ventriculitis 3. Haemorrhage : fresh clot , or adhesive arachnoiditis 4. Cerebral swelling with subfalcine herniation

Subependymal Giant cell astrocytoma

Subependymal giant cell astrocytoma

Central Neuocytoma

Colloid cyst

Colloid cyst

Subfalcine Herniation :

Causes of Thid Ventricle Obstruction:

1. Intraventricular Tumor 2. Extraventricular tumour : Pituitary adenoma , craniopharyngioma, arachnoid cyst.

Pituitary Adenoma

Craniopharyngioma :

Causes of Cerebral Aqueduct of Sylvius Obstruction:

1. Developmental aqueduct stenosis 2. Intraventricular tumour: epndymal seedling 3. Extraventricular Tumour : Pineal Body tumour 4. Ventriculitis 5. Haemorrhage

Aqueduct of Sylvius Obstruction

Pineal Body Tumours:

Pineal Body Tumour:

4th Ventricle obstruction :

1. Intraventricular Tumour: Ependymoma, metastases 2. Extraventricular Tumours: medulloblastoma, haemangioblastoma, cerebellopontine angle tumours (acoutic neuroma) , meningioma 3. Outflow obstrction: infection (TB), SAH, leptomeningeal malignancy

Ependymoma

Medulloblastoma :

Cerebellar Haemangioblastoma

Intraventricular Haemorrhage:

Acoustic Neuroma:

CONGENITAL HYDROCEPHALUS
Intrauterine infection   Rubella Cytomegalo virus Toxoplasmosis

Intra cranial and Intra ventricular haemorrhage Congenital malformations    Aqueduct stenosis, Dandy Walker Syndrome, Arnold Chiari Syndrome, Midline tumors obstructing CSF flow

DANDY WALKER MALFORMATION

 1. 2. 3. Triad of Cystic dilatation of fourth ventricle Cerebellar vermian dysgenesis Hydrocephalus

 Approximately 90% of patients have hydrocephalus, and a significant number of children have associated anomalies, including agenesys of the posterior cerebellar vermis and a corpus callosum.

Chiari Malformation
Consists of two major subgroups: 1. Type I Produces symptoms during adolescence or adult life and is usually not associated with hydrocephalus. The deformity consists of displacement of the cerebellar tonsils into the cervical canal.

Chiari Malformation
2. Type II

Is characterized by progressive hydrocephalus and a myelomeningocele. This lesion represents an anomaly of the hindbrain, probably due to a failure of pontine flexure during embryogenesis, and result in elongation of the fourth ventricle and kinking of the brain stem, with displacement of the inferior vermis, pons, and medulla into the cervical canal.

ACQUIRED HYDROCEPHALUS
Tuberculosis,Chronic & pyogenic Meningitis Post IVH Posterior Fossa tumorsMedulloblastoma,Astrocytoma,Ependymoma Arterio-Venous malformation,Intra cranial haemorrhage,ruptured aneurysm. Hydrocephalus ex vacuo

PATHOPHYSIOLOGY
 The pathophysiology of hydrocephalus is complex.  Together with gross macroscopic changes , HCP also leads to changes in normal physiology , circulation , metabolism ,biochemistry , maturation & ultra structure of brain.  Three factors are basic for the determination of severity & out come.They are age at onset, etioloigy,& duration of disease.

The pathogenesis of hydrocephalus is still poorly defined,despite significant scientific advances and improved understanding of basic cellular mechanisms during health and disease. 1) Cell adhesion molecule L1 (L1CAM), the only gene recognized to cause human hydrocephalus. L1CAM is a single transmembrane molecule involved in neuronal cell adhesion, neurite outgrowth and pathfinding, neuronal migration and myelination, and memory/learning. 2) Transforming growth factor [S]1 (TGF-[S]1), a multifunctional cytokine. Overexpression of TGF[S]1 in the transgenic mouse brain has been shown to cause severe hydrocephalus. The mechanism is related to increased production of extracellular matrix

3) Forkhead/winged helix, member of a large family of evolutionarily conserved DNAbinding proteins. Disruption of this gene causes severe hydrocephalus in a mouse model (mechanism unknown). 4) Otx2, a head organizer during morphogenesis. The heterozygotic mice of mutant Otx2 gene develop hydrocephalus, with edematous changes of the periventricular white matter. This mechanism is also unclear.

There are basic three mechanism involved in hydrocephalus 1. Over production of CSF. 2. Defective absorption of CSF into circulation 3. Blockage of CSF outflow in ventricle or subarachnoid space. As a result fluid accumulated in the ventricles will lead to brain damage either through formation of internal or external hydrocephalus

PATHOLOGICAL EFFECTS OF VENTRICULAR ENLARGMENT

 1.Atrophy of white matter.  2.Spongy edema of brain sorrounding ventricles.  3.Fibrosis of choroid plexus.  4.Stretching & denuding of ependymal epithelium.  5.formation of ventricular diverticula.  6.Fenestration of septum pellucidum.  7.Thinning & elongation of interhemispheric fissure.

 Gross morphologic changes-cause distortion of surrounding structures , thinning of cortical mantle & compression of nearby structure.  Cerebral blood vessels & blood flow damaged due to compression & distortion due to enlarging ventricles , both the superficial & deep blood vessels are affected.  Capillary densities are significantly decreased ,specially around periventricular brain matter.  Also damage to plexus of sympathetic nerves around blood vessels are demonstrated.  TCD s have showed decrease in cerebral perfusion in presence of decompensated HCP . However infarction is rarely seen in association with HCP.

PATHOPHYSIOLOGY

Changes in cerebral circulation

 Increased venous pressure  Delayed emptying of cerebral veins  Narrowing of cerebral arteries  Prolongation of circulation time  Reduced cerebral blood flow  Lowering of CMRO2  Reduced glucose metabolism

PATHOPHYSIOLOGY
 Brain metabolism-decrease in cerebral perfusion ,significantly affect the metabolism as availability of O2 & glucose is decreased.HCP ,then leads to state of sustained hypoperfusion , leaving cerebral tissue vulnerable to hypoxia & ischemia.  In congenital HCP, myelination is severely affected.This change is least reversible to treatment.

PATHOPHYSIOLOGY
 White matter injury occurs by 1) traction on axons & tracts by enlarging venticles 2) by ischemia , because of decreased perfusion .  Injury to cortical neurons are subtle even in presence of gross thinning of mantle  There is thinning & at last fenestation & damage to corpus callosum.

Ventricular distention : Dilation of the lateral ventricles results in stretching of the Corticopontocerebellar and corticospinal pathways, which sweep around the lateral margins of these ventricles to reach the cerebral peduncles. ICP: Manifestations of increased ICP may evolve slowly in obstructive hydrocephalus when there is time for tarnsependymal absorption of CSF to compensate partially for the obstruction, or they may evolve acutely when compensation is absent.

ACUTE HCP
 Phenomenon of acute HCP depends on continued production of CSF with blocked drainage & absorptive pathway.  Lateral ventricles-frontal & occipital horns enlarge first because of least resistance by sorrounding tissue.Then ventricular system enlarges in downward sequence until the site of obstruction is reached.  When full available space is consumed, the stretched epindymal epithelium develops rents & tears edema of white matter .
 Cerebral, IV or cerebellar hematoma ,Paraventricular tumors,Gunshots,Subarachanoid hemorrhage, Acute head injuries, Shunt malfunction.

Subependymal CSF permeation

Chronic HCP
 Compensatory mechanisms in chronic HCP  Expansion of skull  Contraction of cerebral vascular volume  White matter atrophy and ventricular enlargement  Decreased rate of CSF formation.  Diversion of CSF flow to alternative pathways

Clinical Manifestations
The clinical presentation of hydrocephalus is variable and depends on many factors, including : The age at onset. The nature of the lesion causing obstruction. The duration and rate of rise of the ICP. The clinical manifestation of hydrocephalus are caused by ventricular distention and increased ICP.

 The patient of hydrocephalus develop symptoms due to raised ICP.  Headache which is raised in early morning or on lying down .  Vomiting, nausea, papilledema, sleepiness, or coma.  Elevated intracranial pressure may result in uncal and/or cerebellar tonsil herniation, with resulting life threatening brain stem compression.  Further symptoms depend on the cause of the blockage, the person's age, and how much brain tissue has been damaged by the swelling.  In infants with hydrocephalus, CSF fluid builds up in the central nervous system, causing the fontanelle (soft spot) to bulge and the head to be larger than expected.  Eyes that appear to gaze downward-pressure on region of suprapineal recess .  Seperated sutures  Diplopia and blurred vision-6th nerve palsy  Irritability  Spastic paraperesis with exaggerated reflexes  Sleepiness  Blindness-occlusion of PCA,papilloedema,chiasmalcompression

Symptoms that may occur in older children

The presentation in older children is more acute.Features include: Brief shrill and high pitched cry Changes in personality, memory and ability to think or reason Changes in facial expression and eye spacing Crossed eyes and uncontrolled eye movements Difficult feeding, Excessive sleepiness Loss of bladder control Loss of coordination and trouble walking Muscle spasticity Slow growth(0-5years) and restricted movements

Patient of hydrocephalus develop raised ICP Papilledema (more in old children) Cracked pot/Macewan sign(old children) Sixth nerve palsy Impaired upgaze Focal neurological deficits Impaired concious level IN INFANTS Progressive macrocephaly Bulging anterior fontanelle Dilated scalp veins Sun setting signs

Hydrocephalus ex vacuo Normal pressure hydrocephalus

It is compensatory enalargement of cerebral ventricles and subarachnoid space due to brain atrophy or loss of brain parenchyma not the result of increased ICP.  Can occur in post traumatic brain injuries and even in some psychiatric disorders, such as schizophrenia

A chronic type of communicating hydrocephalus Presents mainly in elderly The increase in intracranial pressure (ICP) due to accumulation of cerebrospinal fluid (CSF) becomes stable and that the formation of CSF equilibrates with absorption. CSF pressure reaches a high normal level of 150 to 200 mm of H2O. This phenomenon may be due to a change in compliance (elasticity) of the ventricular walls

Because of this equilibration, patients do not exhibit the classic signs of increased intracranial pressure such as headache, nausea, vomiting, or altered consciousness. patients do exhibit the classic triad of gait difficulties, urinary incontinence, and mental decline It is often misdiagnosed as Parkinsons disease, Alzhiemer disease, and senility due to its chronic nature and its presenting symptoms 2 types a) Idiopathic b) Secondary is due to subarachnoid haemorrhage, head injury, cranial surgery, or CNS infection.

Pathophysiology
 Ventricle enlargement leads to periventricular ischemia regardless of etiology  Compression and stretching of arterioles and venules  Arterial hypertension and cerebral arteriosclerosis increased in NPH

NPH may exhibit the classic triad (also known as Adam's triad) of urinary incontinence, gait disturbance, and dementia 1)Gait disturbance and Ataxia  is the first symptom of the triad Progressive Occurs due to expansion of the ventricular system(particularly at the level of the lateral ventricles)  traction on the lumbosacral motor fibers unsteadiness and impaired balance, especially on stairs and curbs.

NPH gait disturbance is often characterized as a "magnetic gait," in which feet appear to be stuck to the walking surface until wrested upward and forward at each step. 2) Dementia  is predominantly frontal lobe in nature,  with apathy, dullness in thinking, slight inattention. and Memory problems. The dementia is thought to result from traction on frontal and limbic fibers that also run in the periventricular region 3) Urinary incontinence  appears late in the illness, consisting of increased frequency and urgency.

 Pediatric hydrocephalus- By Giuseppe Cinalli, Wirginia June Maixner, Christian Sainte-Ros  Molecular Biology and Genetics of Hydrocephalus=Pattisapu, Jogi MD; Cai, Xingang MD( Issue: Volume 47(2), August 2000, p 525).  Youmans neurological surgery.  Neurosurgery-Sethi S.Rengachary.  Greeneberg Hand book of neurosurgery.  Snells Neuroanatomy.

REFERENCES.

Set of structures containing CSF in brain which is continuous with central canal of spinal cord. Composed of 4 ventricles: 2 Lateral ventricles Third ventricle Fourth ventricle

Derived embryologically from central canal of neural tube

Normal ventricles

Dilated ventricles

In foetus fontanelle and sutures are opened. Posterior fontanel - at birth. Anterior fontanel at 18 months. In initial 6 months of life brain expands at a greater rate. Opened sutures and fontanelle provide proper space for growth of brain and make the skull pliable. If ther is accumulation of fluid in brain of neonate,the increased pressure causes whole skull to swell. Fontanelle bulges and sutures remain seperated and this presents as macrocephaly. Hence MACROCEPHALY and OPEN FONTANELLE provide EARLY DIAGNOSIS in infants.

CHIARI TYPE I MALFORMATION

Chiari type I malformation is the caudal displacement of the cerebellar tonsils below the foramen magnum. Gives symptoms in adolescence or adult life(headache,neck pain, myelopathy) The brain stem and lower cranial nerves are normal .
CHIARI TYPE II MALFORMATION

Progressive hydrocephalus and myelomeningocele. Elongation of IV ventricle Involves caudal displacement of the lower brain stem and stretching of lower cranial nerves Symptomatic patients may be treated with suboccipital craniectomy.

Spina bifida is a developmental birth defect caused by incomplete closure of embryonic neural tube.

DANDY WALKER SYNDROME

Cystic expansion of 4th ventricle in the posterior fossa Developmental failure of roof of the 4th ventricle during embryogenesis. 90% have hydrocephalus. Prominent occiput.

 The patient of hydrocephalus develop symptoms due to raised ICP.  Headache which is raised in early morning or on lying down .  Vomiting, nausea, papilledema, sleepiness, or coma.  Elevated intracranial pressure may result in uncal and/or cerebellar tonsil herniation, with resulting life threatening brain stem compression.

 Further symptoms depend on the cause of the blockage, the person's age, and how much brain tissue has been damaged by the swelling.  In infants with hydrocephalus, CSF fluid builds up in the central nervous system causing the fontanelle (soft spot) to bulge and the head to be larger than expected  Eyes that appear to gaze downward  Seperated sutures  Diplopia and blurred vision  Irritability  Seizures  Sleepiness

Symptoms that may occur in older children The

presentation in older children is more acute.Features include: Brief shrill and high pitched cry Changes in personality, memory and ability to think or reason Changes in facial expression and eye spacing Crossed eyes and uncontrolled eye movements Difficult feeding, Excessive sleepiness Loss of bladder control Loss of coordination and trouble walking Muscle spasticity Slow growth(0-5years) and restricted movements

Patient of hydrocephalus develop raised ICP

Papilledema (more in old children) Cracked pot/Macewan sign(old children) Sixth nerve palsy Impaired upgaze Focal neurological deficits Impaired concious level IN INFANTS Progressive macrocephaly Bulging anterior fontanelle Dilated scalp veins Sun setting signs

NPH may exhibit the classic triad (also known as Adam's triad) of urinary incontinence, gait disturbance, and dementia 1)Gait disturbance and Ataxia  is the first symptom of the triad Progressive Occurs due to expansion of the ventricular system(particularly at the level of the lateral ventricles)  traction on the lumbosacral motor fibers unsteadiness and impaired balance, especially on stairs and curbs.

NPH gait disturbance is often characterized as a "magnetic gait," in which feet appear to be stuck to the walking surface until wrested upward and forward at each step.

2) Dementia  is predominantly frontal lobe in nature,  with apathy, dullness in thinking, slight inattention. and Memory problems. The dementia is thought to result from traction on frontal and limbic fibers that also run in the periventricular region 3) Urinary incontinence  appears late in the illness, consisting of increased frequency and urgency.

 A physician selects the appropriate diagnostic tool based on an individuals age, clinical presentation or type of hydrocephalus and the presence of known or suspected abnormalities of the brain or spinal cord.  Hydrocephalus is diagnosed through 1. Clinical neurological evaluation 2. Lumbar puncture 3. Cranial imaging techniques ultrasonography, computed tomography (CT), magnetic resonance imaging (MRI) and T2 weighted MRI 4. Other ICP-monitoring techniques.

1) CLINICAL NEUROLOGICAL EVALUATION  Signs symptoms and neurological examination with accurate serial recording of head circumference will point towards the diagnosis.  An increase in head circumference in 1st three months of life >1cm every fortnight should arouse suspicion of hydrocephalus  Persistent widening of squamo parietal sutures is not physiological and should arouse suspicion of hydrocephalus.

2)LUMBAR PUNCTURE
a)Obstructive hydrocephalusThis is a contraindication for LP because of the risk of causing tonsillar herniation and death. b)Non Obstructive hydrocephalusLP here may be both diagnostic-by measurement of opening pressure therapeutic-by draining volume of csf c) NPH LP is usually the first step in diagnosis. In most cases, CSF pressure is usually above 155 mmH2O. i) CSF tap test: Clinical evaluation is done before and after removal of CSF (30 ml or more).It has a high predictive value for subsequent success with shunting. This is called the "lumbar tap test" or Miller Fisher test. A "negative" test has a very low predictive accuracy, as many patients may improve after a shunt in spite of lack of improvement after CSF removal. ii) CSF infusion studies :Infusing saline into the thecal sac while measuring tha pressure to obtain and estimate of resistance to CSF outflow>14mmHg/ml/min have a positive predictive value for responsiveness to ventriculoperitoneal shunt insertion.

3) IMAGING STUDIES:
a) Uitrasonography(USG)  Serial USG helps to support the clinical diagnosis and to evaluate serial ventricular size. b) CT Scan and MRI  Ventricular size can be assessed more accurately with CT scan.  Information about cortical mantle, periventricular ooze and etiology of hydrocephalus like Arnold chiari and dandy walker malformation  In children CT shows COPPER BEATING of skull because of chronic raised ICP.  MRI/CT may be necessary to determine site of obstruction and in congenital hydrocephalus to identify associated malformation.  MRI provide better anatomical detail of lesion and is particularly helpful in diagnosis of aqueductal stenosis  Imaging however cannot differentiate between pathologies with similar clinical picture like Alzheimer's dementia, vascular dementia or Parkinson's disease.

Copper beating appearence

Arnold chiari malformation

c) MID LINE T2 WEIGHTED MRI scan Can be used to assess the suitability of patient for third ventriculostomy by identifying the relationships of floor of third ventricle,basilar artery and clivus.

d) ICP MONITORING With a parenchymal probe placed into the frontal lobe via a twistdrill burrhole is a useful diagnostic tool for patients in whom hydrocephalus or CSF shunt dysfunction is suspected.

Hydrocephalus is to be differentiated from conditions manifesting as large heada) MEGANCEPHALY-causes includeHurlers syndrome Metachromatic leukodystrophy Taysachs disease b)CHRONIC HAEMOLYTIC ANAEMIA-(widening of diploic bones) c) VITAMINE D DEFICIENCY d) SUB DURAL EFFUSION e) CEPHALHEMATOMA f) CAPUT SUCCEDENUM g)OTHER CAUSES- HYDRANENCEPHALY,RICKETS,FAMILIAL MACROCEPHALIES

As we have seen that due to blockage of CSF outflow or defective absorbtion or overproduction of CSF,there is accumulation of fluid in ventricles which leads to brain damage and produce signs and symptoms of increased ICP. Only congenital form can be screened by proper antenatal check ups & investigaions. It is diagnosed by neurological evaluation, Imaging, Lumbar Puncture, & ICP monitoring. Only definitive treatment is SHUNTING of CSF either into Peritoneal(VP shunt) or Pleural cavity. A team work of Gynaecologist, Paediatrician, Psychiatrist, Physiotherapist and most importantly Parents is required to combat this problem.

ANATOMY OF PROSTATE
Embryology-Primitive Urethra Anatomical Relations Various Zones Microscopy Applied Anatomy

Anatomy Sagittal section Prostate

Anatomy Transverse Section

PHYSIOLOGY
Hormonal Influences-TestosteronLeydigcell - Lutinising hormone -LHRH -Growth factors Prostate specific antigen- 4 nmol/ml

AETIOPATHOLOGY
Increase Oestrogenic Effects Int. Peptide Growth factors Adenosis,Epitheliosis,Stromal proliferation Lateral & Median lobes Symptoms,BPH,BOO Effects on Urethra & Bladder

Relations of BOO,BPH,Symptoms

Consequences of BPH

Effect on Urethra & Bladder

Bladder effect

CLINICAL FEATURES
LUTSymptoms Voiding - Hesitency, Poor flow - Int stream, dribbling - Sensation of poor emptying - Episod of near retention Storage - Frequency,Urgency,Nocturia - Urge incontinence, Nocturnal inc

CLINICAL FEATURES
Acute retention of urine Chronic retention of urine Haematuria Impaired bladder emptying-Infection & Stone - Pain,Burning mic Renal failure Prostatism

EXAMINATION
Abdominal Examination- Full Bladder External genitalia Per Rectal Examination- Size - Consistency - Tenderness - Rectal mucosa Residual urine measurement

INVESTIGATIONS
Routine blood count Routine urine test, Urine culture Blood urea & s.creatinin, PSA X-ray KUB, USG,Endo USG,IVP Cystoscopy Uroflometry- >15ml/sec for 200 ml void Urodynamics- Pressure flow < 60 cm H2O

IVP

Uroflometry

Urodynamics

Ultrasonography

Endo Rectal USG

D D OF BLADDER OUTFLO OBSTRUCTION

BPH Bladder neck stenosis Bladder neck hypertrophy Prostate cancer Urethral stricture Neuropathic condition-functional obstruction Idiopathic detrusor overactivity

TREATMENT
Conservative -Mild symptoms -Reasonable flow rate > 10ml/se -Residual urine <100 ml Drugs used -Alfa adrinergic blockers -5 Alfa-reductase inhibitors

TREATMENT
Counselling for Prostatectomy -Retrograde ejaculation -Erectil impotence -Success rate-Retention cases do well -BOO 65% scccess -Reoperation- 15% after 8-10 yrs turp -Morbity-Infection,Haematuria in 15%

TREATMENT
Operative -Prostatectomy Approach -TURP Cautry,Laser,Hyperther -RPP -TVP -Perineal Prostatectomy - Stenting

Approaches

TURP

STENTING

COMPLICATION
Haemorrhage Perforation Sepsis Incontinence Retrograde ejaculation Impotence Urethral stricture -Bl Neck Contracture -Reoperation -CVS & RS -Water intoxication -Osteitis pubis

THANKYOU