Hyperglycemia syndromes

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Diabetic Ketoacidosis
Metabolic Acidosis

Insulin Deficiency is the primary defect in patients with DKA

Insulin Deficiency
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.

Persistent Catabolism
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   

Hyperosmolar State
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
Vomiting (50-80%)
 K├╝ssmaul 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
Lethargy, delirium
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.

Semen Analysis

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Assessment of fertility
Forensic purposes
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

Macroscopic Examination
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

Assisted reproductive technology (ART) is a general term referring to methods used to achieve pregnancy by artificial or partially artificial means. It is reproductive technology used primarily in infertility treatments.Examples of ART include in vitro fertilisation, intracytoplasmic sperm injection (ICSI), cryopreservation, and intrauterine insemination (IUI).
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.

Chronic ulceration
Arterial:Atherosclerosis,Buerger’s Disease,Vasculitis,Raynaud’s Disease
Venous:Chronic venous insufficiency,Varicose Veins,Post Sclerotherapy               
Lymphatic:Chronic Lymphodema   

Infective:Pyogenic,Osteomyelitis,Synergistic Gangrene,Syphilis,Tuberculosis,Tropical Diseases,Fungal Diseases
Neoplastic:Melanoma,Kaposi’s Sarcoma
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
 Claudication/rest pain
Risks-Hypertension, smoking, cholesterol, diabetes, exercise
Previous arterial interventions

History of autoimmune disease
Lack chronic arterial occlusive symptoms
Systemic symptoms of autoimmune disease

Previous malignancy
 UV radiation
 Ionising radiation

The Examination of an Ulcer
 Atrophic Skin & Nails                      
 Poor capillary return                       
 Beurger’s angle                           
 Absent pulses, thrills, bruits

 varicose veins                                   

Diabetic Foot Infections

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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
  • Neuropathy
  • Angiopathy
  • 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
Bullae, necrobiosis
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

Motor Neuropathy
Architectural deformities
 Hammer or claw toe
 High plantar arch
 Subluxation of metatarsals

Clinical presentation
 Presence of purulence
 Pain, swelling, ulceration, sinus tract formation, crepitation
 Systemic infection (fever, rigors, vomitting, tachycardia, change in mental status, malaise)
 Surprisingly uncommon
 Metabolic disorder (hyperglycemia, ketosis, azotemia)
 Should be considered even when local signs are less severe

Over the last decade, transvaginal mesh has become widely used in the treatment of pelvic organ prolapse (POP). Constructed of surgical mesh, transvaginal mesh is a medical device that is inserted through the vagina during POP surgery and permanently implanted for the purpose of reinforcing damaged pelvic floor tissues. These devices were cleared by the Food and Drug Administration (FDA) for use in POP treatment in 2002. 

However, as these implants came into popular use, reports of serious complications associated with transvaginal mesh procedures began to emerge. As those reports have increased in numbers dramatically over the past three years, they have raised significant concerns about the safety of treating POP with transvaginal mesh.
Pelvic Organ Prolapse
A very common pelvic floor disorder, POP affects about half of all childbearing women. It is the result of weakening and stretching in the muscles and connective tissues of the pelvic floor, which is the structure that holds pelvic organs, like the uterus and rectum, in place.
POP happens when the pelvic floor becomes too weak to perform that function, allowing one or more of those organs to drop and place pressure on the vagina. While the condition is not life-threatening, severe cases of POP can cause significant interference in bladder, bowel and sexual function. Corrective surgery in such cases can restore a woman's quality of life.
Pelvic Organ Prolapse and Transvaginal Mesh Procedures
The use of transvaginal mesh in POP repair procedures has become prevalent in recent years. These devices generally come in the form of prepackaged kits configured for specific types of POP, many made in a hammock-like design to support prolapsed organs. They are inserted into the pelvic cavity through the vagina and are meant to become a permanent fixture to enhance pelvic support. In 2010 alone, these devices were implanted in 75,000 American women for the treatment of POP.
Transvaginal Mesh and the FDA
Transvaginal mesh was cleared for use in POP treatment through the FDA's 510(k) process, which approves medical devices based on “substantial equivalence” to a product already on the market. This streamlined approval process often requires no clinical evidence to be provided on safety and efficacy.
In the years following FDA approval, as use of these devices increased, so too did reports of serious complications. In 2008, the FDA released a safety alert on transvaginal mesh, advising medical practitioners and patients of complications with the use of mesh implants. In an update to that safety alert, released in 2011, the FDA stated that reports of serious complications had risen five-fold since that 2008 alert.
According to the 2011 update, the most frequently reported complications were mesh erosion, protrusion through vaginal walls, organ perforation, recurrent prolapse, neuro-muscular problems, mesh shrinkage and vaginal scarring. These complications can result in pain, infection, bleeding, sexual dysfunction and urinary problems. 
Many women have required revision surgery due to these issues, and those procedures are not always effective in reliving their symptoms. Some women must live with the complications for the rest of their lives; many women have even filed transvaginal mesh lawsuits against mesh manufacturers to seek compensation for their injuries. The FDA advises that most POP cases can be resolved without the use of mesh, and urges surgeons and patients to consider traditional POP repair as a safer alternative to the use of transvaginal mesh implants.

1.Concept of minimally invasive surgery – classic example like laparoscopic cholecystectomy.
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.

To reduce
  post-operative pain
  tissue destruction & edema
  intra-operative blood loss
Improved  early  mobility
Reduced hospital stay
Cosmetic scar

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

 Cosmetic Value
 Reduced Bleeding , Tissue Damage , Edema
 Less  Pain -  Painless Hysterectomy
 No Intestinal Handling
 No Bladder Drainage
 Early Mobility - No Dvt
 Early Discharge
 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 .
 Restricted Visibility.

Approach to Renal Disorders

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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
Myeloma Kidney
HIV Nephropathy

Renal Biopsy
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

Percutaneous Endoscopic Gastrostomy (PEG): Indications
Long-term feeding
 Mechanical Dysfunction
   Esophageal obstruction
   Swallowing disorder
   Facial fractures
 Neurologic impairment
   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
Gastric volvulus

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
Necrotizing Fasciitis
Gastrocolocutaneous Fistula

Cholestatic Liver Disease

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Adult Cholestatic Liver Disease
  • Primary Biliary Cirrhosis
  • Primary Sclerosing Cholangitis
  • Intrahepatic cholestasis
  • GVHD liver
  • TPN induced cholestasis
  • Sarcoidosis
  • idipathic ductopenia
  • Liver transplant rejection
  • Cystic fibrosis
  • AIDS cholangiopathy
Pediatric cholestatic diseases
  • Cystic fibrosis
  • Alagille’s syndrome
  • Biliary atresia
  • Byler’s disease
  • Inborn errors of metabolism
Liver disease in cholestasis
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

Pathophysiology of renal failure

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The most important functions of the kidney
To keep osmotic pressure
To regulate salt and water balance
To excrete metabolic byproducts
To excrete toxic compounds
Acid-base regulation
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

Hepatorenal syndrome
Atheroembolic renal disease
Renal vein thrombosis

Consequences of acute renal failure
Thirst feeling increases-
 Increased fluid intake
 Hyposmotic hypervolaemia
 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.

Diabetes mellitus
HIV nephropathy
renal artery stenosis and small vessel disease
hemolytic-uremic syndrome and vasculitis
lupus nephritis
drug and toxin-induced chronic tubulointerstitial nephritis and reflux nephropathy
Obstructive such as with bilateral kidney stones and diseases of the prostate


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Patients Selection For Kidney Transplanatation
All patients with end stage renal disease (ESRD) are condidates for KT unless
Systemic malignancy   
Chronic infection.
Severe cardiovascular disease.
Neuropsychiatric disorder
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.

ABO incompatibility.
Cystoxic antibodies against HLA antigens of donor.
Recent or metastatic malignancy.
Active infection.
Severe extrarenal disease (cardiac, pulmonary, hepatic).
Active vasculitis or glomeulonephritis.
Uncorrectable lower urinary tract disease.
Psychiatric illness including alcoholism and drug addiction.
Morbid obesity.
Age > 70 years.
Primary oxalosis.
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.

Endometriosis: The presence of endometrial glands and stromal tissue outside the uterus.
The presence of this ectopic tissue evokes an estrogen-dependent chronic inflammatory process.

Pathological Types
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?
Pelvic tenderness                            
Fixed retroverted uterus
Tender uterosacral ligaments                
Enlarged ovaries

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.

Invasive Diagnosis(Laparoscopy)
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.

The student will
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

Hypoxia, hypercarbia, acidosis
CAD/valvular disease
Systemic hypertension
Ventricular interdependence
Alterations in intrathoracic pressure

Common Sexually Transmitted Diseases

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Genital Ulcer Diseases
  Genital herpes simplex
  Lymphogranuloma venereum
  Granuloma inguinale

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)
mucous patches
condylomata lata - HIGHLY INFECTIOUS
constitutional symptoms
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

Chlamydia trachomatis
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
  Conjunctivitis, pneumonia

Perioperative fluid management

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The goal of perioperative fluid management is to provide the appropriate amount of parenteral fluid to maintain adequate:
Intravascular fluid volume,
Left ventricular filling pressure,
Cardiac output,
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

Vaginal Hysterectomy

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First Clamp
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.

It has now been well established that the management of fractures of  femur in the adolescent age group  are best managed by  reduction and  secure internal fixation rather than non surgical conservative sort of treatment .This results in better outcomes including quicker healing  and the less  eventful complication of  avascular necrosis (AVN)  of the head of femur and length discrepancy , earlier ambulation and weight bearing, better psychosocial results and shortened hospital stay. Subtrochanteric fractures of the femur implement more challenges in management as they hold limited ability to compensate for malalignment with the presence of deforming muscle forces.
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

Hyperthyroidism and Thyroid Storm

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Normal Thyroid State
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

Thyroid Storm
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

Syndrome of Inappropriate ADH Secretion
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.

SIADH: causes
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

Diabetes Insipidus
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...

Pelvic Organ Prolapse

Posted by e-Medical PPT

DeLancey’s three levels of vaginal support
Apical suspension       
 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
Estrogen deprivation
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

Uterine prolapse
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

External Cephalic Version

Posted by e-Medical PPT

Spontaneous version
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.
1% IUFD.
Spontaneous reversion.

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.
Un-engaged breech.

Multiple pregnancy.
APH, P.Praevia.
Ruptured membranes.
Significant foetal abnormalities.
Need for CS for other indications.
Tocolysis is C/I in congenital or acquired heart disease, DM or thyroid disease.

Previous CS.
Severe protienuric PIH.
RH iso-immunization.
(Evidence of macrosomia).

USS to confirm normal baby and normal AFV.
Reactive CTG.
Informed concent: PTL, ROM,cord and placental accident.
Facilities for immediate CS.
Kleihauer test.

Primary Objective:  The physician should be able to stabilize, evaluate, and treat the comatose patient in the emergent setting.
The physician should understand this involves an organized, sequential, prioritized approach.

Primary Objectives
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.

Secondary Objectives
The physician should understand and recognize:
 Herniation syndromes
 Signs of supratentorial mass lesions
 Signs of subtentorial mass lesions
The physician should be able to develop the differential diagnosis of metabolic coma.

Consciousness requires:
 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

Herniation Syndromes
Central herniation
 Rostral caudal progression of respiratory, motor, and pupillary findings
 May not have other focal findings
Uncal herniation
 Rostral caudal progression
 CN III dysfunction and contralateral motor findings

Sepsis_Pathophysiology and Treatment

Posted by e-Medical PPT

Systemic Inflammatory Response Syndrome (SIRS) :
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.
Cardiovascular :
SBP<90mmhg/MAP<70 for at least 1 hr despite adequate volume resuscitation or the use of vasopressors to achieve the same goals.
Renal :
Urine output <0.5ml/kg/hr or Acute Renal Failure.
Pulmonary :
PaO2/FiO2 <250if other organ dysfuncton is present or <200 if the lungs is the only dysfunctional organ.
Gastrointestinal :
Hepatic dysfunction (hyperbilirubinemia,Elevated transaminases
Alteration in Mental status (delirium)
Hematologic :
Platelet count of <80,000/mm3 or decreased by 50% over 3 days/DIC
Metabolic :
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.

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