Insulin Deficiency is the primary defect in patients with DKA
Breakdown of storage forms of energy to meet energy needs. (Catabolism)
Gluconeogenesis (from amino acids, lipids)
Glucagon unopposed by Insulin stimulates this catabolic reaction
Skeletal and cardiac tissues are able to use free fatty acids and ketone bodies as an energy source.
Glucose can not be used by these tissues in the absence of insulin.
The brain is an insulin-independent tissue and continues to use available glucose.
Hyperglycemia is worsened by further intake of glucose.
Excess Ketone bodies from Lipolysis
Ratio of hydroxybutyrate (BHB)/Acetoacetate (AA) normally 3:1 is driven to 15:1 in severe DKA
Hyperglycemia acts as an osmotic diuretic with obligatory loss of water and electrolytes.
Ketosis/hyperglycemia stimulate vomiting with aggravation of dehydration
Hypovolemia secondary to dehydration can promote decreased tissue perfusion with anaerobic metabolism and elevated lactate production
Total fluid deficit in severe DKA usually averages around 10% of the total body weight
Clinical Findings in DKA
Polyuria, Polydipsia, Polyphagia
Dehydration + orthostasis
Küssmaul respiration if pH < 7.2
Temperature usually normal or low, if elevated think infection!
Abdominal pain present in at least 30%.
Clinical Findings of Hyperosmolarity
Hyperosmolar coma is the first sign of diabetes in 50-60 % of adult patients.
Hyperglycemia usually > 700-800mg/dl
Osmolarity above 340 mOsm/L is required for coma to be present.
Assessment of fertility
Effectiveness of vasectomy - 2 samples 1 month apart negative
Suitability for artificial insemination
Semen Analysis Include
Macroscopic:viscosity,coagulation + liquifaction,volume,pH
Motility and Viability must be performed within 1½ - 2 hrs of collection
Semen is viscous, yellow grayish.
Forms gel-like clot immediately.
Liquefies completely in 5-60 minutes; this must be complete before further testing (mix before further testing).
Appearance: homogenous white-gray opalescence.
Brown/red in hematospermia
Dense white turbid if inflammation and high WBC
Volume: in graduated cylinder to the nearest 0.1 ml or centrifuge tube free of contamination.
Viscosity: 5ml pipette or plastic pipette
normal, more viscous, very viscous
pH:important parameter of motility and viability 7.2-8.0; measured by pH paper.
Aspermia: No semen ejaculated
Hematospermia: Blood present in semen
Leucocytospermia: White blood cells present in semen
Azospermia: No spermatozoa found in semen
Normospermia: Normal semen parameters
Oligospermia: Low sperm concentration
Asthenospermia: Poor motility and/or forward progression
Teratospermia: Reduced percentage of morphologicall normal sperm
Necrospermia: No live sperm in semen
In vitro fertilization (IVF) is the technique of letting fertilization of the male and female gametes (sperm and egg) occur outside the female body.Techniques usually used in in vitro fertilization include:
Transvaginal ovum retrieval (OCR) is the process whereby a small needle is inserted through the back of the vagina and guided via ultrasound into the ovarian follicles to collect the fluid that contains the eggs.
Embryo transfer is the step in the process whereby one or several embryos are placed into the uterus of the female with the intent to establish a pregnancy.
Artificial insemination (AI) is when sperm is placed into a female's uterus (intrauterine) or cervix (intracervical) using artificial means rather than by natural copulation.
The majority of IVF-conceived infants do not have birth defects.However, some studies have suggested that assisted reproductive technology is associated with an increased risk of birth defects.
The main risks are:
Genetic disorders. DNA damage increases in e.g. IVF and ICSI
Low birth weight.
Preterm birth. Low birth weight and preterm birth are strongly associated with many health problems, such as visual impairment and cerebral palsy, and children born after IVF are roughly twice as likely to have cerebral palsy.
Arterial:Atherosclerosis,Buerger’s Disease,Vasculitis,Raynaud’s Disease
Venous:Chronic venous insufficiency,Varicose Veins,Post Sclerotherapy
Infective:Pyogenic,Osteomyelitis,Synergistic Gangrene,Syphilis,Tuberculosis,Tropical Diseases,Fungal Diseases
Systemic-Metabolic:Ulcerative Colitis,Diabetes,Sickle Cell Disease,Avitaminosis
Neurotrophic:Cord Lesions,Peripheral Neuropathies,Trauma,Diabetes,Tabes dorsalis,Alcoholism
The history of an ulcer
Chronic ischaemic symptoms
Risks-Hypertension, smoking, cholesterol, diabetes, exercise
Previous arterial interventions
History of autoimmune disease
Lack chronic arterial occlusive symptoms
Systemic symptoms of autoimmune disease
The Examination of an Ulcer
Atrophic Skin & Nails
Poor capillary return
Absent pulses, thrills, bruits
Cellulitis occurs 9 times more frequently in diabetics than non-diabetics
Osteomyelitis of the foot 12 times more frequently in diabetics than non-diabetics
Foot ulcerations and infections are the most common reason for a diabetic to be admitted to the hospital
25 % of diabetics will develop a foot ulcer
40-80% of these ulcers will become infected
25 % of these will become deep
50 % of patients with cellulitis will have another episode within 2 years
10-30 % of patients with a diabetic foot ulcer will go on to amputation
- Metabolic derangement
- Faulty wound healing
- Mechanical stress
- Patient and provider neglect
Poor Wound Healing
Poor granuloma formation
Prolonged persistence of abscess
Higher rate of carriage of Staph Aureus in the nares
Nail fungi (Tenia)
Poor Immune Function
Poor PMN functions
Migration, phagocytosis, intracellular killing, chemotaxis
Ketosis impairs leukocyte function
Monocyte mediated immune function diminished
Hyperglycemia impairs complement fixation
Hammer or claw toe
High plantar arch
Subluxation of metatarsals
Presence of purulence
Pain, swelling, ulceration, sinus tract formation, crepitation
Systemic infection (fever, rigors, vomitting, tachycardia, change in mental status, malaise)
Metabolic disorder (hyperglycemia, ketosis, azotemia)
Should be considered even when local signs are less severe
2.Laparoscopic Hysterectomy introduced in 90’s
3.Advantages of Laparoscopic Hysterectomy
4.Majority of Gynaecologists / patients – rural / semi urban areas – NOT able to afford the cost
5.Benefits of laparoscopic surgery minus increased cost, complications & instrumentation.
tissue destruction & edema
intra-operative blood loss
Improved early mobility
Reduced hospital stay
Around 4-5 Cm(1.5 ” To 2 ”) Mini-pfannestiel Incision - Taken In Pubic Hair-line
Obliquely Pulling, Left Cornu Delivered
Uterus Turned To Left & By Pull, Right Cornu Delivered Out
“obliquely Pull-turn-pull-push Action ”
Uterus & Adnexae Delivered Out Of Abdomen
Use Of Small C-shaped & Right Angled Retractors , Instead Of Self Retaining Ones.
Rest Steps Of Hysterectomy Same As In Routine - Vaginal Closure, Peritonization .
Largest Removed Uterus - 4” In Breadth
Reduced Bleeding , Tissue Damage , Edema
Less Pain - Painless Hysterectomy
No Intestinal Handling
No Bladder Drainage
Early Mobility - No Dvt
Early Resumption Of Daily Core
Not Possible In -
Large Fibroids , Large Solid Ovarian Masses
Grossly Obese Patients (upto 100 Kg Patients Have Beeen Operated)
Multiple Abdominal Surgeries (many Previous 2-3 Lscs Patients Have Been Operated)
Delivering Uterus Out Difficult - Needs Skill, Maneuverability And Practice .
To identify appropriate strategies for investigation of the patient with kidney disease
To discuss interventions that may alter the course of disease
To discuss indications for referral to a nephrologist
Elevated Serum creatinine: recommendations for management and referral. CMAJ 1999: 161:413-17
National Kidney Foundation: Kidney Disease Outcomes Quality Initiative (NKF-KDOQI), 2002
Practice guidelines for Chronic Kidney Disease. 2003. Annals of Internal medicine. Vol. 139 Number 2.
Workup of a decreased GFR
1. Identify chronicity (Acute vs chronic)
2. Identify the cause, especially reversible causes
3. Identify Indications for Referral to a Nephrologist
4. Initiate a cause specific management plan in a multidisciplinary team.
Normal size kidneys in chronic kidney disease
Polycystic kidney disease
Should be considered:
If noninvasive tests have failed to establish a diagnosis in a patient with:
Nephrotic syndrome (except in DM or established amyloid)
Non-nephrotic proteinuria if associated with renal dysfunction
Lupus nephritis (for dx and staging)
Acute nephritic syndrome
Unexplained acute/ subacute renal failure
To direct and evaluate effectiveness of therapy
Management of Renal Disease
Treatment of Reversible Causes
Preventing or Slowing Progression
Treating and Preventing the Complications
Identifying Individuals Requiring Renal Replacement Therapy
Closed head injury
Replace nasoenteric feeding tube
Reduce risk of aspiration, sinusitis
Facilitates tube replacement for mechanical problems
Permit transfer to long term facility
Decompressive tube for palliation (carcinomatosis,gastric obstruction, severe diabetic gastroparesis)
Access for repeated endoscopic or surgical instrumentation (e.g. bougie)
Recirculation of bile-Fistula, biliary drain
Poorly selected populations have 30 day mortality of up to 50% after PEG
Exception: palliative, for decompression
Inability to perform upper endoscopy
Obstructing esophageal tumor
Inability to appose gastrotomy to anterior abdominal wall
Previous subtotal gastric resection
Hepatomegaly, esp left lobe
Complications of PEG
Pneumoperitoneum and Peritonitis
Dislodgement of PEG Tube
Buried Bumper Syndrome
Peristomal Wound Infection
- Primary Biliary Cirrhosis
- Primary Sclerosing Cholangitis
- Intrahepatic cholestasis
- GVHD liver
- TPN induced cholestasis
- idipathic ductopenia
- Liver transplant rejection
- Cystic fibrosis
- AIDS cholangiopathy
- Cystic fibrosis
- Alagille’s syndrome
- Biliary atresia
- Byler’s disease
- Inborn errors of metabolism
Mediated by high levels of toxic bile acids
Preferential retention of hydrophobic bile acids
Direct damage to hepatocytes and bile duct cells
Lithocholic and chenodeoxycholic acids are toxic
Degree of liver damage related to bile acid level
Damage to cell membranes, necrosis
Cholestasis may lead to immune activation
Mechanism is probably multifactorial
Initial immunologic insult
Bile duct loss and failure to transport bile acids
Retention of hydrophobic bile acids
Cholate, chenodeoxycholate accumulate
further direct and immune-mediated damage
Clinical complications of cholestasis
Pruritus very common and may be disabling
Exact mechanism unknown
Possible relationship with bile acid levels
Fat malabsorption and steatorrhea
Fat-soluble vitamin deficiencies (A, D, E, K)
Marked elevation in cholesterol levels
Xanthomas and xantholesmas
Early and severe osteoporosis may occur
Laboratory tests in cholestatic disease
Very high serum alkaline phosphatase, GGT
Less striking elevation in other liver enzymes
Serum bilirubin is elevated late in the disease
Four stages of disease:
one: no symptoms
two: fatigue and pruritus
three: liver fibrosis and elevated bilirubin
four: cirrhosis and liver failure
To keep osmotic pressure
To regulate salt and water balance
To excrete metabolic byproducts
To excrete toxic compounds
Endocrine function (erythropoetin, etc)
Synthesis of enzymes and regulatory compounds
Definition of acute renal failure
It develops in days or weeks
It can be best characterized as a serious decrease in the glomerular filtration (GFR).
Prerenal-blood supply failure
Postrenal-obstruction of the urinary system
Intrinsic (40%)-damage to the kidney itself
Atheroembolic renal disease
Renal vein thrombosis
Consequences of acute renal failure
Thirst feeling increases-
Increased fluid intake
Edema - hyponatraemia
Disturbed H+ excretion - metabolic acidosis
Increase in plasma urea and creatinine concentrations
Thromboses, anemia, hemolysis
Plasma phosphate conc. increases,Plasma Ca++ level decreases
Chronic renal failure
Slow but irreversible death of nephrons, accompanied by a continuous decrease of renal function.
renal artery stenosis and small vessel disease
hemolytic-uremic syndrome and vasculitis
drug and toxin-induced chronic tubulointerstitial nephritis and reflux nephropathy
Obstructive such as with bilateral kidney stones and diseases of the prostate
All patients with end stage renal disease (ESRD) are condidates for KT unless
Severe cardiovascular disease.
Extremes of age (relative)
Patient Survival After Kidney Transplantation VS haemodialysis
Annual mortality rates for patients under dialysis range from 21%-25%, but <8% with cadaveric and <4% with living-related transplant recipients.
Healthier patients generally are selected for transplantation.
The benefit of transplantation is most notable in young people and in those with diabetes mellitus.
Principles Involved In evaluating A Prospective Living Kidney Donor
Whether there is a medical condition that will put donor at increased risk for complications for general anesthesia or surgery.
Whether the removal of one kidney will increase the donor’s risk for developing renal insufficiency.
CONTRAINDICATIONS TO RENAL TRANSPLANTATION
Cystoxic antibodies against HLA antigens of donor.
Recent or metastatic malignancy.
Severe extrarenal disease (cardiac, pulmonary, hepatic).
Active vasculitis or glomeulonephritis.
Uncorrectable lower urinary tract disease.
Psychiatric illness including alcoholism and drug addiction.
Age > 70 years.
Persistent coagulation disorder.
Does Donation Of A kidney Pose A long-term Risk For The Donor?
Following nephrectomy, compensatory hypertrophy and increase in GFR occur in the remaining kidney.
Slight risk of poteinuria and hypertension.
Meta-analysis of data from donors followed for >20y confirmed safety of kidney donation.
The presence of this ectopic tissue evokes an estrogen-dependent chronic inflammatory process.
Peritoneal endometriosis: (superficial implant)
Ovarian endometriomas: (Chocolate Cyst)
Deeply infiltrating disease: (extend >5 mm beneath the peritoneum) usually affects bowel, bladder and ureters.
What Are The Suggestive Signs of Endometriosis?
Fixed retroverted uterus
Tender uterosacral ligaments
The diagnosis is more certain if:
Deeply infiltrating nodules are palpated on the US ligament or in the D. pouch.
Visible lesions are seen in the vagina or on the cervix.
Non Invasive Diagnosis
The use of transvaginal ultrasound is helpful in diagnosing ovarian endometriomas.
The use of serum CA-125 testing has limited value as a screening test for endometriosis.
Laparoscopy is the 'gold standard' diagnostic test in endometriosis
Less Invasive Method Mini-laparoscopy
Is Histological Confirmation Necessary for Diagnosis of Endometriosis?
Visual inspection is usually adequate but histological confirmation of at least one lesion is ideal.
In cases of ovarian endometrioma (> 3 cm in diameter), and in deeply infiltrating disease, histology should be obtained to identify endometriosis and to exclude rare instances of malignancy.
Correlate physiological comorbidity issues with the anesthesia care plan
List position considerations specific to these surgical procedures
Describe the use of DLT and general considerations
Identify factors to prevent exacerbation of pulmonary vasoconstriction
CLINICAL Symptom &Signs:Pulmonary hypertension, RVH, Cor Pulmonale
Prominent neck veins, prominent A waves& perhaps prominent V waves on EKG
Prominent left parasternal heave & rocking motion synchronous with heartbeat may be noted
Auscultate: pulmonary component of 2nd heart sound increases
High pitched, early systolic ejection click
Systolic ejection murmur
R-sided atrial S4 gallop indicating inc RVEDP
Middiastolic R-sided S3 gallop, usually clear evidence of impaired RV function. Differentiated: gallops inc in intensity with
Early diastolic, pulmonary regurg murmur ind functional impair secondary to dilation of PA root
Rt heart failure with chronic dependent edema, large tender liver, ascites, dilated distended neck veins
CXR in Pulmonary HTN
Main pulmonary vessels dilated
Characteristic of COPD with hyperinflated lungs, low flat diaphragm
Evidence of RVH; clockwise cardiac rotation, loss of air space behind the sternum on a lateral view
LV DYSFUNCTION CONTRIBUTORS
Hypoxia, hypercarbia, acidosis
Alterations in intrathoracic pressure
Genital herpes simplex
Primary Syphilis - Clinical Manifestations
Incubation: 10-90 days (average 3 weeks)
Early: macule/papule erodes
Late: clean based, painless, indurated ulcer with smooth firm borders
Unnoticed in 15-30% of patients
Resolves in 1-5 weeks
Secondary Syphilis - Clinical Manifestations
Represents hematogenous dissemination of spirochetes
Usually 2-8 weeks after chancre appears
rash - whole body (includes palms/soles)
condylomata lata - HIGHLY INFECTIOUS
Sn/Sx resolve in 2-10 weeks
Gonorrhea - Clinical Manifestations
Urethritis - male
Incubation: 1-14 d (usually 2-5 d)
Sx: Dysuria and urethral discharge (5% asymptomatic)
Dx: Gram stain urethral smear (+) > 98% culture
Urogenital infection - female
Endocervical canal primary site
70-90% also colonize urethra
Incubation: unclear; sx usually in l0 d
Sx: majority asymptomatic; may have vaginal discharge, dysuria, urination, labial pain/swelling, abd. pain
Dx: Gram stain smear (+) 50-70% culture
Responsible for causing cervicitis, urethritis, proctitis, lymphogranuloma venereum, and pelvic inflammatory disease
Direct and indirect cost of chlamydial infections run into billions of dollars
Potential to transmit to newborn during delivery
Intravascular fluid volume,
Left ventricular filling pressure,
Systemic blood pressure,
and ultimately, oxygen delivery to tissues
Rational approach to fluid management
In addition to surgical considerations (blood loss, evaporative loss, third spacing), certain conditions and changes that occur during the perioperative period can make the management of fluid balance a challenge, including preoperative:
fluid volume status, preexisting disease states,and the effect of anesthetic drugs on normal physiology
Management of fluid therapy
Management of fluid therapy may influence intraoperative and postoperative morbidity and mortality.
Providing sufficient intravascular fluid volume is essential for adequate perfusion of vital organs.
Although quantitative considerations are of primary concern, oxygen carrying capacity, coagulation, and electrolyte and acid-base balance are also of critical importance.
Preoperative assessment of intravascular fluid volume is important before induction of anesthesia.
Common causes of preoperative hypovolemia:
Bowel preparations, vomiting, diarrhea, diaphoresis, hemorrhage, burns, and inadequate intake
Redistribution of intravascular fluid volume without evidence of external loss is another important cause of preoperative volume depletion.
Examples: patients with sepsis, adult respiratory distress syndrome, ascites, pleural effusions, and bowel abnormalities.
Often, these processes are accompanied by increased capillary permeability resulting in loss of intravascular fluid volume to interstitial and other fluid compartments.
Evaluation of intravascular fluid volume relies on indirect measurements such as systemic blood pressure, heart rate, and urine output because measurements of fluid compartments are not readily available.
Even with sophisticated monitoring techniques (pulmonary artery catheters, arterial oxygen saturation), the adequacy of intravascular fluid volume replacement and tissue oxygen delivery to individual vital organs cannot be precisely determined.
For these reasons, clinical evaluation of intravascular fluid volume is necessary
After pushing up the bladder and opening the pouch of Douglas (POD), 1st clamp is applied to uterosacral ligament as close to the uterus as possible; Confirming that the inside blade is inside the peritoneal cavity to include the small vessels between the peritoneum and the base of the pelvis
First ligatures is left with long threads, one with needle will be used to have a bite in the lateral vaginal angle so:
Support the vaginal vault by ligating it to the main supporting structures of the pelvis
Shares in the homeostasis of that vascular area
2nd Ligatures, Step ladder
Almost always the 2nd bite will not reach the level of uterine vessels and we don’t intend to do so.
The long thread of the 1st bite is tied with one of the threads of the next ligature so the whole uterosacral was at the end taken to the vaginal angle.
The whole three pedicles are ligated together on one side with marked stitch. During peritonization, one thread from round ligament was tied to its counterpart on the other side and peritoneum was approximated
At the end, The pedicles are sutured to the vagina:
That vaginal angle was sutured to the uterosacral ligaments as a first step, giving a strong support to vaginal vault at the end of operation, preventing vault prolapse.
In 1998, the average charge for a laparoscopically-assisted vaginal hysterectomy in the united states was $14,500; An abdominal hysterectomy was $12,500: that for a vaginal hysterectomy was $10,380; And that for (stat bull Metrop Insur co 2000).
Vaginal hysterectomy resulted in better quality-of-life outcomes and lower costs compared with laparoscopically assisted vaginal or abdominal hysterectomy (van den Eeden 1998).
Vaginal hysterectomy should be considered whether there is associated prolapse or not.
With proper selection, continued training, its rate will increase in front of abdominal or laparoscopic route.
Good access and assessment of uterosacrals.
Good support to the vagina.
There is a lack of agreement regarding definition of the fractures .
Mathew and Jeffrey: it is subtrochanteric femoral fracture in pediatrics when the fracture distance is less than 10% from lesser trochanter compared to total shaft length , an area in which the muscle deforming action results in difficulty to control reduction
Modalities of internal fixation include:
. titanium elastic nails (TEN)
. cephalomedullary nails (CM)
. interlocking nails
. Smith Peterson plates
. plate and hip screw
. nail and intramedullary hip screw and cancellous screws.
For the management of this injury we use trochanteric antigrade nail (TAN), a rigid intramedullary nail with a trochanteric entry point
Purpose is to decrease wound dissection and to provide secure fixation that will enhance ambulation and full weight bearing which in turn will make a more satisfactory post-operative period, thus a quicker return to pre-operative activities, and augment bone healing
Synthesis and release of thyroid hormone is controlled by TSH relaesed form the anterior pituitary
TSH is controlled by the release of thyroid releasing hormone (TRH) from the hypothalmus and a negative feedback loop to the pituitary
Thyroid hormone production s dependent on adequate adequate iodine intake
Thyroid hormone is reversible bound to various proteins including thyronine-binding globulin (TBG)
Free unbound portions are biologically active
T4 is the predominant circulating hormone
T4 is deiodinated to t3
T3 is biologically more active than T4 but has a shorter half-life
Occurs in in all ages
Uncommon under the age of 15
10 x’s more common in women (1/10,000)
Graves disease is the most common etiology
80% of cases in the U.S.
Common in the 3rd and 4th decades
Caused by autoimmune thyroid-stimulating antibodies
Associated with diffuse goiter, opthalmopathy, and local dermopathy
Toxic multinodular and toxic nodular goiters are the next most common etiologies
Usually occurs in older populations
Commonly with previous history of goiter
Often with milder symptoms of thyrotoxicosis
Amiodarone-induced thyrotoxicosis (AIT)
Amiodarone is iodine rich and may cause both hyper and hypothyroidism
Difficult to treat because of incomplete understanding of mechanism
Two major forms exists
Type 1 occurs with a normal thyroid
Type 2 occurs with a abnormal thyroid
Tx. Varies based on the the type
Confirmed by thyroid function test
Elevated free T4 and Low TSH
In some cases of graves disease T4 may be normal and TSH decreased but the patient appears thyrotoxic
T3 level should be done to rule out T3 toxicosis
Hypothyroidism secondary to pituitary adenoma will have elevated TSH levels
A life threatening hypremetabolic state due to hyperthyroidism
Mortality rate is high (10-75%) despite treatment
Usually occurs as a result of previously unrecognized or poorly treated hyperthyroidism
Thyroid hormone levels do not help to differentiate between uncomplicated hyperthyroidism and thyroid storm
Definition: levels of ADH are inappropriately elevated compared to body’s low osmolality, and ADH levels are not suppressed by further decreases in blood osmolality.
Irritation of CNS: meningitis, encephalitis, brain tumors, brain hemorrhage, hypoxic insult, trauma, brain abscess, Guillain Barre, hydrocephalus
Pulmonary disorders: pneumonia, asthma, positive end expiratory pressure ventilation, CF, TB, pneumothorax
Unregulated tumor production of ADH-like peptides: oat cell lung carcinoma for example, Ewings sarcoma, carcinoma of duodenum, pancreas, thymus
Function of ADH
ADH is made in the supra-optic nuclei in the hypothalamus, stored in the posterior pituitary
Normally released into the bloodstream when osmo-receptors detect high plasma osmolality
At the kidney, attaches to receptors in the collecting ducts, opens up water channels
Water is passively reabsorbed along the kidney’s medullary concentration gradient
SIADH: signs and symptoms
Signs of hyponatremia: lethargy, apathy, disorientation, muscle cramps, anorexia, agitation
Signs of water toxicity: nausea, vomiting, personality changes, confused, combative
Definition: inability to effectively conserve urinary water
Central: ADH not made or not released in the hypothalamic-pituitary axis
Nephrogenic: ADH is released but not detected by the receptors in the kidney collecting ducts, often a sex-linked recessive condition, also due to renal pathology, electrolyte disorders, drugs...
Upper paracolpium suspends apex to pelvic walls and sacrum
Damage results in prolapse of vaginal apex
Midvaginal lateral attachment
Vaginal attachment to arcus tendineus fascia and levator ani muscle fascia
Pubocervical and rectovaginal fasciae support bladder and anterior rectum
Avulsion results in cystocele or rectocele
Distal perineal fusion
Fusion of vagina to perineal membrane, body and levators
Damage results in deficient perineal body or urethrocele
Mutifactorial involving both neuromuscular and endopelvic fascial damage
Relaxation of the tissues supporting the pelvic organs may cause downward displacement of one or more of these organs into the vagina, which may result in their protrusion through the vaginal introitus.
Factors promoting prolapse
Erect posture causes increased stress on muscles, nerves and connective tissue
Acute and chronic trauma of vaginal delivery
Intrinsic collagen abnormalities
Chronic increase in intraabdominal pressure
Main support of urethra and bladder is the pubo-vesical-cervical fascia
Essentially a hernia in the anterior vaginal wall due to weakness or defect in this fascia
Midline weakness allows bladder to descend causing central cystocele
Tearing of endopelvic fascial connections from lateral sulci to arcus tendinii causes lateral or displacement cystocele
Detachment of pubocervical fascia from pericervical ring causes a transverse or apical cystocele
Symptoms include pelvic pressure and bulge or mass in the vagina
Surgical repair is treatment of choice.Anterior Colporrhaphy,Paravaginal repair and Colpocleisis are the surgical treatment options
Normal cervix located in upper third of vagina
Degree of prolapse measured by position of cervix at maximum intraabdominal pressure, without traction
Complete uterovaginal prolapse is called procidentia
After 32/40 is as high as 57% and after 36/40 may still be as high as 25%.
Is more in multiparous.
Less likely in primipara and extended breech.
Risks of ECV
Severe bradycardia requires immediate delivery by CS.
Benefits to fetus
Decreases the risks of foetal trauma.
Decreases the incidence of cord prolapse.
Decreases the rate of unattended breech delivery.
Any breech after 36/40.
Significant foetal abnormalities.
Need for CS for other indications.
Tocolysis is C/I in congenital or acquired heart disease, DM or thyroid disease.
Severe protienuric PIH.
(Evidence of macrosomia).
USS to confirm normal baby and normal AFV.
Informed concent: PTL, ROM,cord and placental accident.
Facilities for immediate CS.
The physician should understand this involves an organized, sequential, prioritized approach.
Treatment of rapidly progressive, dangerous metabolic causes of coma (hypoglycemia)
Evaluation as to whether there is significant increased ICP or mass lesions.
Treatment of ICP to temporize until surgical intervention is possible.
The physician should understand and recognize:
Signs of supratentorial mass lesions
Signs of subtentorial mass lesions
The physician should be able to develop the differential diagnosis of metabolic coma.
An intact pontine reticular activating system
An intact cerebral hemisphere, or at least part of a hemisphere
Coma requires dysfunction of either the:
Pontine reticular activating system, or
Bihemispheric cerebral dysfunction
Supratentorial lesions cause coma by either widespread bilateral disease, increased intracranial pressure, or herniation.
Infratentorial lesions involve the RAS, usually with associated brainstem signs
Metabolic coma causes diffuse hemispheric involvement and depression of RAS, usually without focal findings
Rostral caudal progression of respiratory, motor, and pupillary findings
May not have other focal findings
Rostral caudal progression
CN III dysfunction and contralateral motor findings
Systemic inflammatory response to various stresses.
Meets 2 or more of the following criteria :
Temperature of >38C/<36degree C
Heart rate of more than 90 beats/min
RR >20 breaths/min or PaCo2 <32mmHg
WBC >12,000/mm3 or <4000/mm3
Evidence of SIRS accompanied by known or suspected infection.
Severe SEPSIS :
Sepsis accompanied by hypoperfusion or organ dysfunction.
SBP<90mmhg/MAP<70 for at least 1 hr despite adequate volume resuscitation or the use of vasopressors to achieve the same goals.
Urine output <0.5ml/kg/hr or Acute Renal Failure.
PaO2/FiO2 <250if other organ dysfuncton is present or <200 if the lungs is the only dysfunctional organ.
Hepatic dysfunction (hyperbilirubinemia,Elevated transaminases
Alteration in Mental status (delirium)
Platelet count of <80,000/mm3 or decreased by 50% over 3 days/DIC
PH<7.30 or base deficit >5.0mmol/L
Plasma lactate >1.5 upper limit of normal.
Septic Shock :
Severe Sepsis with persistent hypoperfusion or hypotension despite adequate fluid resuscitation
Multiple Organ Dysfunction Syndrome (MODS)
MODS occurs late and is the most common cause of death in patients with Sepsis.
Lactic acidosis led investigators to think that this is due to tissue ischaemia.
Minimal cell death in postmortem samples taken from the failed organs of patients with Sepsis.
Recovery from Sepsis is associated with near complete recovery of organ function, even in organs whose cells have poor regenerative capacity.
Increased tissue oxygen tensions in various organs (muscle, gut, bladder) in animals and patients with Sepsis.