ECG 3-Normal Sinus Rhythm (NSR)



•    Etiology: the electrical impulse is formed in the SA node and conducted normally.

•    This is the normal rhythm of the heart; other rhythms that do not conduct via the typical pathway are called arrhythmias.


NSR Parameters
•    Rate                60 - 100 bpm   
•    Regularity            regular
•    P waves            normal
•    PR interval            0.12 - 0.20 s
•    QRS duration        0.04 - 0.12 s
Any deviation from above is sinus tachycardia, sinus bradycardia or an arrhythmia



Arrhythmia Formation
Arrhythmias can arise from problems in the:
•    Sinus node
•    Atrial cells
•    AV junction
•    Ventricular cells


SA Node Problems
The SA Node can:
fire too slow--- Sinus Bradycardia

fire too fast--- Sinus Tachycardia




Atrial Cell Problems
Atrial cells can:

•    fire occasionally from a focus ---Premature Atrial Contractions (PACs)

•    fire continuously due to a looping re-entrant circuit ----Atrial Flutter



Atrial Cell Problems
Atrial cells can also:
• fire continuously from multiple foci Atrial Fibrillation

or
fire continuously due to multiple micro re-entrant “wavelets” Atrial Fibrillation




AV Junctional Problems
The AV junction can:

•    fire continuously due to a looping re-entrant circuit--Paroxysmal   Supraventricular Tachycardia
•    block impulses coming from the SA Node--AV Junctional Blocks



Ventricular Cell Problems
Ventricular cells can:
•    fire occasionally from 1 or more foci --Premature Ventricular Contractions (PVCs)
•    fire continuously from multiple foci--Ventricular Fibrillation
•    fire continuously due to a looping re-entrant circuit--Ventricular Tachycardia

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ECG 2 -How to Analyze a Rhythm


• Step 1: Calculate rate.
• Step 2: Determine regularity.
• Step 3: Assess the P waves.
• Step 4: Determine PR interval.
• Step 5: Determine QRS duration.





Step 1: Calculate Rate

• Option 1
– Count the # of R waves in a 6 second rhythm strip, then multiply by 10.
– Reminder: all rhythm strips in the Modules are 6 seconds in length.

Interpretation? 9 x 10 = 90 bpm



• Option 2

– Find a R wave that lands on a bold line.
– Count the # of large boxes to the next R wave. If the second R wave is 1 large box away the rate is 300, 2 boxes - 150, 3 boxes - 100, 4 boxes - 75, etc.
– Memorize the sequence:
300 - 150 - 100 - 75 - 60 - 50



Step 2: Determine regularity

• Look at the R-R distances (using a caliper or markings on a pen or paper).
• Regular (are they equidistant apart)? Occasionally irregular? Regularly irregular? Irregularly irregular?

Interpretation? Regular




Step 3: Assess the P waves

• Are there P waves?
• Do the P waves all look alike?
• Do the P waves occur at a regular rate?
• Is there one P wave before each QRS?
Interpretation? Normal P waves with 1 P wave for every QRS



Step 4: Determine PR interval

• Normal: 0.12 - 0.20 seconds.
(3 - 5 boxes)

Interpretation?0.12 seconds



Step 5: QRS duration

• Normal: 0.04 - 0.12 seconds.
(1 - 3 boxes)
Interpretation? 0.08 seconds



Rhythm Summary

• Rate 90-95 bpm
• Regularity regular
• P waves normal
• PR interval 0.12 s
• QRS duration 0.08 s
Interpretation?  Normal Sinus Rhythm

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ECG 1-Basics

Normal Impulse Conduction
Sinoatrial node--AV node--Bundle of His--Bundle Branches--Purkinje fibers




The “PQRST”
►    P wave - Atrial   depolarization


        QRS - Ventricular    depolarization
        T wave - Ventricular   repolarization




The PR Interval
Atrial depolarization
+
delay in AV junction
 (AV node/Bundle of His)

 (delay allows time for the atria to contract before the ventricles contract)



Pacemakers of the Heart
►    SA Node - Dominant pacemaker with an intrinsic rate of 60 - 100 beats/minute.

►    AV Node - Back-up pacemaker with an intrinsic rate of 40 - 60 beats/minute.

►    Ventricular cells - Back-up pacemaker with an intrinsic rate of 20 - 45 bpm.



The ECG Paper


►    Horizontally
    One small box - 0.04 s
    One large box - 0.20 s
►    Vertically
    One large box - 0.5 mV

►    Every 3 seconds (15 large boxes) is marked by a vertical line.
►    This helps when calculating the heart rate.

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Drug therapy in Diabetes



Aims  of management
►    To achieve near normal glycaemia
-    Short term- to prevent symptoms of hyper & hypo
-    Long term- to prevent complications
►    Good quality of life, near normal life expectancy



Types of Insulin
►      Short acting -      Soluble / Neutral insulin
                       Insulin aspart
                     Insulin lispro
►     Intermediate acting - Isophane
►     Long acting - Insulin Zinc suspension
                  new insulin analogue - Glargine
                                 Detemir 
►      Biphasic- mixture of short and intermediate
                     Biphasic lispro
                     Biphasic Isophane


Types of Insulin

Insulin
Lispro
Aspart
Neutral/
regular
Isophane
ultratard
Glargine
Onset
10-20
30
1h
4h
2-4h
Peak
1h
1-3h
4-6h
6-18h
peak less
Duration
3-5h
4-8h
8-14h
24h
20-24h





Soluble insulin / neutral /clear
►    Names - Human actrapid/ Humulin S
►    Species- Bovine, porcine, human
►    Following s/c injection
        Onset of action – 30 min
           Peak- 1-3 hours
           Duration- 4-8 hours
►    Only insulin suitable for intravenous route –plasma half life < 5 min, required continuous infusion
►    Used in diabetes Ketoacidosis


Sites of injections - Subcutaneous
►    Thighs
►    Upper buttocks
►    Abdomen
►    Arms
Important to rotate the site
Rate of absorption may be significantly different – faster from arm and abdomen than from thigh and buttock


Routes of Administration
►    Subcutaneous for long term regular use
►    Intravenous infusion in acute conditions- diabetes Ketoacidosis, Perioperative period, Hyperosmolar Nonketotic state  ONLY NEUTRAL/ CLEAR INSULIN CAN BE USED
►    Continuous subcutaneous insulin infusion via pump – neutral
►    Intraperitoneal – Peritoneal dialysis patients
►    Inhaled insulin- experimental


Untoward effect of insulin
►    Hypoglycaemia
►    Weight gain- anabolic hormone
►    Lipohypertrophy- injection to same site
►    Insulin oedema
►    Transient deterioration in retinopathy
►    Insulin neuritis – actively regenerating neurone, uncommon
►    Postural hypotension



Recurrent Hypo
►    ? Required dose adjustment
►    ? Right insulin/ injection technique
►    ? Meal/ fasting related
►    ? Injections sites
►    ? Exercise
►    Unexplained - ?autonomic neuropathy


Sick day rules
    never stop insulin
    monitor more frequently
    maintain your hydration
    Check for ketones
    Know when & how to call for help


Oral Medications to Treat Type 2 Diabetes
Major Classes of Medications
    sensitize   the body to insulin +/- control hepatic glucose production

    stimulate the pancreas to make more insulin

    slow the absorption of starches

Thiazolidinediones
Biguanides


Sulfonylureas
Meglitinides


Alpha-glucosidase
 inhibitors



Thiazolidinediones
►    ↓ insulin resistance by making muscle and adipose cells more sensitive to insulin. They also suppress hepatic glucose production.
►    Efficacy
    ↓ fasting plasma glucose ~1.9-2.2 mmol/L
    Reduce A1C ~0.5-1.0%
    6 weeks for maximum effect
►    Other Effects
    Weight gain, oedema
    Hypoglycemia (if taken with insulin or agents that stimulate insulin release)
    Contraindicated in patients with abnormal LFT or CHF
    Improves HDL cholesterol and plasma triglycerides; usually LDL neutral
►    Medications in this Class: pioglitazone (Actos), rosiglitazone (Avandia), [troglitazone (Rezulin) - taken off market due to liver toxicity]


Biguanides
►    Biguanides ↓ hepatic glucose production and increase insulin-mediated peripheral glucose uptake.
►    Efficacy
    Decrease fasting plasma glucose 60-70 mg/dl (3.3-3.9 mmol/L)
    Reduce A1C 1.0-2.0%
►    Other Effects
    Diarrhea and abdominal discomfort
    Lactic acidosis if improperly prescribed
    Cause small decrease in LDL cholesterol level and triglycerides
    No specific effect on blood pressure
    No weight gain, with possible modest weight loss
    Contraindicated in patients with impaired renal function
    Medications in this Class: metformin (Glucophage), metformin hydrochloride extended release (Glucophage XR)


Sulfonylureas
►    Sulfonylureas increase endogenous insulin secretion
►    Efficacy
    Decrease fasting plasma glucose 3.3-3.9 mmol/L
    Reduce A1C by 1.0-2.0%
►    Other Effects
    Hypoglycemia
    Weight gain
    No specific effect on plasma lipids or blood pressure
    Generally the least expensive class of medication
►    Medications in this Class:
    First generation : chlorpropamide , tolazamide, acetohexamide , tolbutamide
    Second generation : glyburide , glimepiride , glipizide


Meglitinides
►    stimulate insulin secretion (rapidly and for a short duration) in the presence of glucose.
►    Efficacy
    ↓ peak postprandial glucose
    ↓ plasma glucose 3.3-3.9 mmol/L
    ↓ HbA1C 1.0-2.0%
►    Other Effects
    Hypoglycemia (may be less than with sulfonylureas if patient has a variable eating schedule)
    Weight gain
    No significant effect on plasma lipid levels
    Safe at higher levels of serum Cr than sulfonylureas
►    Medications in this Class: repaglinide , nateglinide


Alpha-glucosidase Inhibitors
►    Alpha-glucosidase inhibitors block the enzymes that digest starches in the small intestine
►    Efficacy
    ↓ peak postprandial glucose 2.2-2.8 mmol/L
    ↓ fasting plasma glucose 1.4-1.7 mmol/L
    Decrease A1C 0.5-1.0%
►    Other Effects
    Flatulence or abdominal discomfort
    No specific effect on lipids or blood pressure
    No weight gain
    Contraindicated in patients with inflammatory bowel disease or cirrhosis
►    Medications in this Class: acarbose , miglitol 




Combination Therapy  for Type 2 Diabetes
Sulfonylurea + Biguanide
    Glyburide  +  Metformin     -  Glucovance
    Glipizide  +  Metformin     -  Metaglip

Thiazolidinedione + Biguanide
   Rosiglitazone + Metformin  -  Avandamet


Chart


Clinic Checklists
►    Glycaemic control- home monitoring, HbA1c, inj site, hypo
►    Diet, exercise, Smoking, alcohol
►    BP
►    Weight
►    Macrovascular- CVA, IHD
►    Microvascular- Retinopathy, microalbuminuria, neuropathy
►    Foot
►    Lipid profile, renal function, TSH


Special circumstances
►    Intercurrent illness
►    Peri-operative period
►    Pregnancy
►    Childhood and adolescents
►    Others- travelling across time zones
                Exercise
                Alcohol
            Driving


Dr K S Myint
Specialist Registrar

SNAKE BITE (INDIAN SCENARIO)


►    3500   SPECIES
►    300     VENOMOUS
►    30000  - 40000 DEATHS ANNUALLY


POISONOUS SNAKES
INDIAN SCENARIO
►    5 DANGEROUSLY POISONOUS SNAKES
          KING COBRA
          COMMON COBRA
          COMMON KRAIT
          RUSSELL’S VIPER
          SAWSCALED VIPER
MOST COMMON POISONOUS SNAKE IS COMMON KRAIT

►    216  SPECIES

►    52  VENOMOUS



SNAKE VENOM
►    Toxic saliva secreted by modified parotid glands of a venomous snake
►    Amber coloured when fresh
►    Constituents               Toxins
                                       Enzymes
                                       Miscellaneous : neurotoxins
                                                                cardiotoxins
                                                                hemolysin


VENOM CLASSIFICATION
►    Neurotoxic              elapids(cobra,krait)
►    Hemotoxic               viperidae
►    Myotoxic                  sea snake
►    Krait and russell’s viper is much more toxic than that of cobra


SYMPTOMATOLOGY OF NON VENOMOUS SNAKES
►    Universal fear associated induce a state of shock
►    Bite site may demonstrate multiple teeth impressions
►    Lack of significant local pain or swelling
►    Adequate reassurance and symptomatic treatment measures lead to full recovery


SYMP..VENOMOUS SNAKE BITES
►    ELAPID BITE
►    Local features :
►        indistinct fang marks ,
►        burning pain,
►        swelling and discolouration,                                                                        
►        serosanguinous discharge

       
Systemic features

►    preparalytic stage  :     emesis,
                                             headache,
                                              LOC.
      paralytic stage      : ptosis,
                                           ophthalmoplegia
                                           drowsiness,
                                           dysarthria,
                                           dysphagia,
                                           convulsions,
                                           bulbar paralysis,
                                           resp failure .

     

VIPERID BITE

Local features:
                         rapid swelling,
                         discolouration,
                         blister formation,
                         bleeding from bite site,
                         severe pain
    
Generalised bleeding manifestations.                       
                          epistaxis,
                          hemoptysis,
                          bleeding gums
                          hemauria
                          purpuric spots
 Renal failure

      

HYDROPHID BITE

►    Local features: minimal swelling and pain
►    Systemic features: myalgia muscle stiffness
                  myoglobinuria , renal tubular
                  necrosis                  


DIAGNOSIS OF SNAKE BITE
►    FANG MARKS:classically, two puncture                wounds seperated by a distance varying from 8mm to 4cm, depending on the species involved.
►    However a side swipe may produce only a single puncture,while multiple bites could result in numerous fang marks.
►    Baileys method
  
      



Management of snake bite

FIRST AID

►    DELAY ENRY OF VENOM
►    TOURNIQUET
►    ABOVE KNEE
►    ABOVE ELBOW


CLINICAL ASSESMENT
►    VITAL SIGNS—PULSE
                           --B P
                           --RESPIRATION –SBC
OBSERVE – BITE MARK
                   --LOCAL REACTION
                   --PAINFUL LNE
►               


NEUROTOXICITY
►    PTOSIS
►    OPHTHALMOPLEGIA
►    MYASTHENIA LIKE SYMPTOMS
►    ASSES SBC



HEMATOTOXICITY

►    PURPURA
►    ECHYMOSIS
►    GINGIVAL SULCUS BLEED
►    HEMATURIA

CAPILLARY LEAK SYNDROME
►    PUFFINESS
►    CHEMOSIS
►    PAROTID SWELLING




Lab. Investigations
  
Haematological-
                             leucocytosis(>20,000-
                                     severe envenomation)                          
                            elevated PCV
                             thrombocytopenia
                             evidence of hemolysis
                             prolonged CT,PT,PTT
                             elevated FDP



►    CT     >    20 MINUTES

►    SURE SIGN OF ENVONOMATION

►    PITVIPER   > 2 WEEKS

►    ECG: bradycardia
             ST    /
             Twave inversion
             QT Prolongation
             changes due to hyperkalemia
             

►    Metabolic
         hyperkalemia
         hypoxemia with resp.Ac
         met.Ac or lactic Ac
►    Urine
         hematuria,proteinuria,Hburia
         Mburia
        


►    Renal : ARF -- BU S.Cr   S E
►    CXR :  pulm.edema
               intrapulm.Hgs
               pleural effusion
►     Immunodiagnosis: by ELISA….
     highly sensitive but specificity inadequate to diff b/w diff species of snakes



SPECIFIC MANAGEMENT  ASV
►    HORSE SERUM
►    ASV IN INDIA
                        COBRA
                        KRAIT
                        RUSSEL’S VIPER
                        SAW SCALED VIPER
 1 mi ASV     ---    0.6m6 cobra R viper
                     ---    0.45mg krait S viper
                       


Indication ---- systemic manifestaiton
►    NEUROTOXICITY
►    REPEATED VOMITING
►    HAEMOTOXICITY
►    NEPHROTOXICITY
►    CARDIOTOXICITY
►    RHABDOMYOLYSIS


►    PROLONGED  CT  ALONE

                       PIT VIPER  --  NO
                       SNAKE NOT IDENTIFIED


NEUROTOXIC ENVONOMATION
►    INITIAL DOSE  10  -  15 VIALS
►    REASSESS
►    IMPROVEMENT   30  --  60 MIN
►    REPEAT  5 VIALS AFTER 60  -- 90 MINS
►    SUPPORTIVE – NEOSTIGMINE AFTER ATROPINE


HAEMOTOXIC ENVONOMATION
►    MILD            CT  <  30 MINS
                        CLOT SIZE  =  50% blood col
                        initial dose  = 5 vials
►    MODERATE   CT   >  30 MINS
►                           CLOTS ONLY SPECKLES
►                           intial dose   = 10 vials
►    SEVERE      INCOAGULABLE
►                         initial dose  = 15 vials


►    REPEAT  CT  AFTER 6 – 9 HOURS
►    IF CT PRONGED REPEAT 5- 10  VIALS
►    LOW DOSE INFUSION – FOLLOWING
                                            DAYS


SUPPORTIVE CARE

  ANTIBIOTICS
  METHYL PREDNISOLONE
  FFP,FRESH BLOOD
  PREVENTION AND Rx OF HYPOTENSION
  PRVENTION OF SHOCK



PREVENTION OF ARF
►    PROPER FLUID ADMINISTRATION
►    CORRECT MYOCARDIAL DYSFUNCTION
►    MONITOR OUTPUT BU S.Cr SE
►    AVOID  NEPHROTOXIC DRUGS
►    PROTEIN RESTRICTION



Management of local reactions
►    BULLAE   - LEFT INTACT
►    NECROSIS  - DEBRIDEMENT
►    COMPARTMENT SYNDROME – FASCIOTOMY
►    MOST COMFORTABLE POSITION


REACTIONS TO ANTIVENOM
►    ANAPHYLACTOID  10 – 90 MINS

►    PYROGENIC 2 HOURS

►    SERUM SICKNESS  5 – 21 DAYS
►    Rx  local anaesthetic ice pack


dr.muhammed faisal

calicut medical college

Diseases of Sclera


Special features of Sclera
•    Avascular
•    Dense fibrous tissue
•    Lack of reaction to insult
•    Two types of inflammation - episcleritis and scleritis



Episcleritis
•    Benign inflammatory affection of deep subconjunctival connective tissue and superficial scleral lamellae
•    Mostly bilateral
•    Dense lymphocytic infiltration
•    Reaction to endogenous toxin
•    Association with rhuematoid arthritis

Symptoms and Signs
•    Young females
•    Acute redness
•    Mild pain
•    No discharge
•    Two types     - simple or diffuse
                        - nodular


Simple /diffuse episcleritis
•    Sectorial or diffuse redness
•    One or both eyes
•    Mild to moderate tenderness over the area of redness
•    Engorgement of large episcleral vessels which run in radial direction beneath the conjunctiva

Nodular Episcleritis


Treatment
•    Mild to moderate- weak topical steroids
•    Fluorometholone eye drops  4 times a day and lubricating drops
•    Severe form - stronger steroids as prednisolone acetate eye drops 4-6 times a day
•    Non steroidal anti inflammatory drugs like-ibuprofen 400 mg thrice daily or indomethacin can be given

Scleritis
•    Extends more deeply
•    Deep lymphocytic infiltration deep with in the scleral tissue
•    Bilateral, rarer, more in females
•   
•    Associated with connective tissue disorder in 50% cases  like - polyarteritis nodosa, SLE, reiters syndrome  ankylosing spondylitis, wegners grannulomatosis, dermatomyositis, polychondritis, gout, herpes zoster ophthalmicus,syphilis
•    Recent ocular surgery as cataract or RD surgery


A. Anterior scleritis
–    Nodular
–    Diffuse
–    Necrotising     - with inflammation                                - without inflammation
B.  Posterior scleritis



Nodular scleritis
•    One or more nodules
•    Less circumscribed than episcleritis
•    First dark red or bluish later becomes purple and semitransparent like porcelain
•    All around cornea-annular scleritis –grave prognosis


Diffuse scleritis
•    Hard whitish nodule pin head size with inflamed surrounding zone
•    Disappear without disintegration



Clinical features of Scleritis
•    Cornea and uveal tract are always involved as contrast to episcleritis
•    Some iritis  more often cyclitis and ant. Choroiditis
•    No ulceration
•    Dark purple weak cicatrix-ciliary staphyloma
•    Secondary glaucoma common


Sclerosing keratitis
•    Extends to cornea
•    Opacity develops at the margin of cornea adjoining scleritis
•    Tongue shaped, rounded apex towards center of cornea
•    No corneal vascularisation or ulceration
•    Pupillary area is usually spared
•    Keratolysis is a serious complication


Necrotizing scleritis
•    Scleral necrosis
•    Severe thinning
•    Melting of sclera
•    Two types    - with inflammation
                       - without inflammation


Necrotizing scleritis with inflammation
•    Red ,painful eye, worsening of symptoms
•    Associated with ant uveitis
•    Autoimmune disorder
•    Complications-glaucom, cataract, sclerosing keratitis, scleral melting are common
•    Five year survival of patients at this stage of autoimmune disorder is 25%


Necrotizing scleritis without  inflammation-
scleromalacia perforans
•    Patients with seropositive rheumatoid arthritis
•    Painless scleral thinning and melting
•    Cause is ischemia


Posterior scleritis
•    Inflammation with thickening of posterior sclera
•    Primary or secondary extension of anterior scleritis
•    Not associated with systemic disease
•    Usually no symptoms


Symptoms and Signs
•    Decreased vision
•    With or without pain
•    Proptosis
•    Restricted ocular movements
•    Post vitritis, disc edema ,macular edema, choroidal detachment exudative retinal detachment
•    B-scan and CT scan shows thickened sclera



Diagnosis – episcleritis / scleritis
•    Full blood count
•    RA factor
•    Mantoux test
•    ANA
•    Anti neutrophill cytoplasmic antibody

•    VDRL
•    Serum uric acid
•    X-ray chest, sacro iliac joint
•    LE cells
•    Full immunological survey for tissue antibodies


Treatment
•    Diffuse and nodular scleritis- NSAID
•    Prednisolone -1mg /kg single morning dose
    Tapered to 20 mg over 2-3 weeks
•    H2 receptor blockers
•    Necrotizing scleritis - additional immunosuppressant are recommended
•    Abundant lubricant
•    Scleral patch graft may be needed if risk of perforation

Posterior scleritis
•    Same as ant scleritis
•    IV Methylprednisolone as pulse therapy
•    Local steroids ineffective
•    SUBCONJUNCTIVAL INJECTIONS CONTRAINDICATED
•    Infectious diseases are treated with appropriate antibiotics

Staphyloma
•    Staphyloma is a clinical condition characterised by an ectasia of the outer coats (cornea,or sclera or both) with an incarceration of uveal tissue
•    Two factors work - weakening of the outer wall and raised IOP

TYPES
•    Anterior
•    Intercalary
•    Ciliary
•    Equatorial
•    Posterior


Anterior staphyloma
•    Partial or total
•    Mostly after sloughed cornea and pseudocornea formation
•    AC becomes flat with secondary glaucoma
•    Iris is incarcerated in anterior staphyloma

Intercalary staphyloma
•    Limbus
•    Root of iris and anterior most part of ciliary body
•    Externally from limbus to 2mm behind
•    Caused by - perforating injury at peripheral cornea involving limbus, marginal corneal ulcers, anterior scleritis, scleromalacia perforans, complicated cataract surgery with wound dehisence, secondary glaucoma


Ciliary staphyloma
•    Affects ciliary zone - upto 8 mm behind the limbus
•    Scleral ectasia with incarceration of ciliary body
•    Caused by - developmental glaucoma, end stage of primary or sec glaucoma, scleritis, trauma to ciliary region of eye


Equatorial staphyloma
•    Equatorial region of eye with incarceration of choriod
•    14 mm behind the limbus weak area due to passage of venae vorticosae
•    Caused by scleritis , chronic uncontrolled glaucoma, degenerative myopia


Posterior staphyloma
•    Posterior pole of eye lined by choroid
•    Degenerative high myopia
•    Detected by fundoscopy and B- scan ultrasonography



Treatment
•    Treat the cause
•    Small –local excision with corneo-scleral graft
•    Large unsightly blind eyes are enucleated and replaced with implant


Dr Kavita Kumar
Associate Professor
Department of Ophthalmology
Gandhi Medical College
Bhopal

Complicated cataract, Cataract associated with systemic diseases and management of Cataract


Complicated Cataract

Cataract associated with ocular diseases:
Complicated Cataract : is due to disturbance of the nutrition of lens due to inflammatory or degenerative disease of anterior and /or posterior segment of the eye like iridocyclitis, cilitis, pars planitis, choroiditis, myopic degeneration, retinitis pigmentosa, retinal detachment, other retinal pigmentory dystrophies etc.

►    A non-descript opacity develops in cortex which usually progresses and mature.
►    In inflammatory or degenerative condition of posterior segment, opacification usually starts in the posterior part of the cortex in the axial region (posterior cortical cataract or posterior subcapsular cataract)

►    Cataract has characteristic breadcrumb appearance and rainbow display of colours (polychromatic lustre). Cataract may remain stationary in posterior cortex or progress to involve the whole posterior cortex and entire lens. Cataract is usually soft and uniform in appearance.
►    Vision is usually affected even in early stages as opacity is near the nodal point of the eye.


Prognosis depends on the causative condition.
►    All cases of cataract without obvious cause should be carefully looked for keratic precipitates or evidences of pars planitis.


Cataract associated with systemic disease
►    Diabetic Cataract:
    Early onset of senile cataract and cataract develops rapidly.
    True diabetic cataract is rare condition, occurring typically in young people with acute diabetes (with gross imbalance of water balance of the body). Fluid droplets (vacuoles) appear under the anterior and posterior subcapsular cortex, manifesting as myopia, producing diffuse opacity. These changes are reversible.

►    The lens rapidly becomes cataractous with dense, white anterior and posterior subcapsular cortical cataract resembling snowstorm “snowflake Cataract”.
►    If diabetes is controlled appropriately, the rapid progression to mature cataract may be arrested.


►    Parathyroid Tetany
►    Myotonic Dystrophy
►    Galactosaemia
►    Down Syndrome
►    Atopic Cataract

Objective Examination
►    The state of the nucleus (grading of nuclear sclerosis)
►    The state of the cortex
►    The presence or absence of signs of inflammation
►    Pupillary glow by transillumination
►    B- Scan ultrasonography


Functional Tests
►    Pupillary reaction
►    Projection of light
►    Macular function test – two pinholes test and Maddox rod test
►    Entoptic view of the retina : Auto-ophthalmoscopy
►    Electro-retinographic record, particularly of macula.

Pre-operative evaluation
►    Thorough ocular examination to exclude any ocular disease like abnormalities of lids, lacrimal sac, conjunctiva (including conjunctival infections), cornea, uveal inflammation, glaucoma, posterior segment inflammatory/ degenerative condition etc.

Systemic examination to exclude hypertension, cardiovascular disorder, cerebro-vascular disease, chronic obstructive air way disorder etc. If any disorder is present, it should be adequately controlled before surgery
►    ENT and Dental checkup to exclude septic focus


Treatment of cataract
►    Medical treatment: No medical treatment is effective once the lens opacity has developed.

►    Surgical Treatment:
Indication for surgery:
    1. Cataract – when routine work becomes difficult due to reduced vision (attributable to cataract)
    2. Subluxated or dislocated lens
    3. Lens induced complications like phacolytic uveitis / glaucoma, phacoanaphylactic endophthalmitis, phacomorphic glaucoma.


►    Surgical Treatment:
    Options
    I. Intracapsular lens extraction (ICCE): Method of intracapsular cataract extraction (ICCE), now becoming obsolete, by which the entire lens including the capsule is removed by rupturing zonular ligaments.

    II. Extracapsular Cataract Extraction (ECCE):
        Methods –
    1. Conventional ECCE
    2. ECCE by small incision cataract surgery (SICS)
    3. Lensectomy
    4. Phacoemulsification
   

Steps of ECCE
•    Anaesthesia
    a. General Anaesthesia : In children, psychiatric patients, senile dementia
    b. Local anaesthesia: Retrobulbar block, peribulbar block, along with or without facial block , topical anaesthesia
   
2. Cleaning of lids with 5% betadine solution and instillation of betadine solution in conjunctival sac
3. Draping
4. Superior Rectus suture in case of conventional ECCE and SICS
5. Conjunctival flap in case of SICS

6. Scleral tunnel incision or Corneo-scleral section or corneal or corneal tunnel incision
7. Anterior chamber entry
8. Injection of ocular viscosurgical device (OVD) in anterior chamber (HPMC or Sodium Hyaluronate)
9. Capsulotomy ( can opener or continuous curvilinear capsulorrhexis, CCC)
10. Hydrodissection and Hydrodelineation
11. Nucleus delivery (in conventional ECCE and SICS) / Phacoemulsification of nucleus (in phacoemulsification, machine , through titanium needle provides energy for emulsification of nucleus, needle vibrates at an speed of 20,000 Hz and pulverizes the nucleus)

12. Cortical clean up by aspiration and irrigation (BSS or Ringer lactate is used as irrigating fluid)
13. Filling of lens capsule (capsular bag) with OVD
14. Insertion of posterior chamber IOL (in the bag, in case of complications in the ciliary sulcus)
15. Removal of OVD from anterior chamber
16. Closure of wound of entry (corneoscleral wound requires sutures 10-0 silk or nylon), phaco and SICS incisions are self sealing.



Complications of Cataract Surgery
•    Due to local anesthesia: Retrobulbar haemorrhage, globe perforataion, oculocardiac reflex etc. 
•    Intra-operative complications : detachment of descemet’s membrane, damage to corneal endothelium, zonular dialysis, posterior capsular rupture

III. Early post-operative complications: wound leak and complications related to it (iris prolapse, flat anterior chamber), secondary glaucoma, postoperative infection, lens matter induced uveitis etc.


IV. Late post-operative complications: cystoid macular edema, posterior capsular opacification, corneal endothelial decompensation causing corneal edema, retinal detachment, displacement of IOL etc.

ECTOPIC PREGNANCY


DEFINITION

Any pregnancy where the fertilised ovum gets implanted & develops in a site other than normal uterine cavity.


INCIDENCE
>1 in 100   pregnancies.
•    Recent evidence indicates that the incidence of ectopic pregnancy has been rising in many countries.
–    USA-5 fold
–    UK-2 fold
–    France 15/1000 pregnancies
–    India-1in100 deliveries
•    Recurrence rate - 15% after 1st, 25% after 2 ectopics


HISTORY

•    Ectopic pregnancy was first described in 963 Ad by Albucasis.
•    1884 -- Robert Lawson Tait of Birmingham prformed the first successful Salpingectomy operation
•    1953 -- Stromme – Conservative surgery of    Salpingostomy
•    1973 -- Shapiro & Adller – Laparoscopic Salpingectomy
•    1991 -- Young et al – Laparoscopic Salpingotomy


AETIOLOGY

•    Any factor that causes delayed transport of  the fertilised  ovum  through the.
•    Fallopian tube favours implantation in the tubal mucosa itself  thus giving rise to a tubal ectopic pregnancy.
•    These factors may be Congenital or Acquired.


•    CONGENITAL - Tubal Hypoplasia , Tortuosity , Congenital diverticuli , Accessory ostia , Partial stenosis
•    ACQUIRED -
–    Inflammatory: PID, Septic Abortion, Puerperal Sepsis, MTP (lntraluminal adhesion)
–    Surgical: Tubal reconstructive surgery, Recanalisation of tubes
–    Neoplastic: Broad ligament myoma, Ovarian tumour
–    Miscellaneous Causes:  IUCD , Endometriosis, ART (IVF & & GIFT), Previous ectopic


CLINICAL PRESENTATION

•    Ectopic Pregnancy remains asymptotic until it ruptures when it can present in two variations - Acute &. Chronic
•    SYMPTOMS-
–    Amenorrhea
–    Abdominal Pain
–    Syncope
–    Vaginal Bleeding
–    Pelvic Mass


DIAGNOSIS

“Pregnancy in the fallopian tube is a black cat on a dark night. It may make its presence felt in subtle ways and leap at you or it may slip past unobserved. Although it is difficult to distinguish from cats of other colours in darkness, illumination clearly identifies it.”           
--Mc. Fadyen - 1981


•    In recent years, inspite of an increase in the incidence of ectopic pregnancy there has been a fall in the case fatality rate.
•    This is due to the widespread introduction of diagnostic tests and an increased awareness of the serious nature of this disease.
•    This has resulted in early diagnosis and effective treatment.
•    Now the rate of tubal rupture is as low as 20%.


METHODS OF EARLY DIAGNOSIS

•    Immunoassay utilising monoclonal antibodies to beta HCG
•    Ultrasound scanning – Abdominal & Vaginal including Colour Doppler
•    Laparoscopy
•    Serum progesterone estimation not helpful


The USG features of ectopic pregnancy after 5 weeks can be any of the following-
•    Poorly defined tubal ring possibly containing echogenic structure and POD typically containing fluid or blood.
•    Ruptured ectopic with fluid in the POD and an empty uterus.
•    In Colour Doppler, the vascular colour in a characteristic placental shape, the so-called fire pattern, can be seen outside the uterine cavity while the uterine cavity is cold in respect to blood flow



MANAGEMENT

•    Depends on the stage of the disease and the condition of the patient at diagnosis.
•    Options-
–    Surgery – Laparoscopy / Laparotomy
–    Medical – Administration of drugs at the site / systemically
–    Expectant – Observation

MANAGEMENT OF ACUTE 
ECTOPIC PREGNANCY
•    Hospitalisation
•    Resuscitation -
–    Treatment of shock
–    Lie flat with the leg end raised
–    Analgesics
–    Blood transfusion

Culdocentesis: -
•    Most Helpful in Emergent Situations to Confirm Diagnosis
•    Highly Specific if performed and Interpreted Correctly: - Presence of Free-Flowing, NON-Clotting Blood
•    Negative Tap Inconclusive
•    Remains Controversial


•    Laparotomy should be done at the earliest.
•    Salpingectomy is the definitive treatment.
•    No benefit from removing Ovary along with the tube
•    If blood is not available, auto-transfusion can be done.


MANAGEMENT OF CHRONIC 
ECTOPIC PREGNANCY

INVESTIGATIONS-
•    Laboratory/Chemical test –
–    Serial quantitative beta HCG level by RIA
–    Serum progesterone level (<5 mg/ml in ectopic pregnancy)
–    Low levels of Trophoblastic proteins such as SPI and PAPP-, Placental protein 14 & 12
•    USG- usually haematocele is found
•    Laparoscopy
MANAGEMENT OF CHRONIC 
ECTOPIC PREGNANCY


TREATMENT – ALWAYS SURGICAL
•    Salpingectomy of the offending tube
•    If pelvic haematocele is infected, posterior. colpotomy is to be done to drain the pelvic abscess
•    Salpingo-oophorectomy


MANAGEMENT OF UNRUPTURED ECTOPIC PREGNANCY
•    SURGICAL-
•    SURGICALLY ADMINISTERED MEDICAL (SAM) TREATMENT
•    MEDICAL TREATMENT
•    EXPECTANT MANAGEMENT


SURGICAL TREATMENT OF ECTOPIC PREGNANCY
•    Carried out either by Laparoscopy / Laparotomy.
•    The procedures are: -
–    Salpingectomy / Cornual resection / Excision
–    Conservative  surgery (in cases of Infertility & desire for pregnancy)
•    Linear salpingostomy
•    Linear salpingotomy
•    Segmental resection and  anastomosis
•    Milking of the tube

LAPAROTOMY? 
VS. 
LAPAROSCOPY?

SALPINGECTOMY?
VS
SALPINGOSTOMY / SALPINGOTOMY?


•    It is carried out by laparoscopic scissors and diathermy or Endo-loop.
•    After passing a loop of No.1 catgut over the ectopic pregnancy the stitch is tightened and then the tubal pregnancy is cut distal to the loop stitch.
•    The excised tissue is removed by piece meal or in a tissue removal bag.

•    To reduce blood loss, first 10-40 IU of vasopressin diluted in10 ml of normal saline is injected into the mesosalpinx.
•    Then the tube is opened through an antimesenteric longitudinal incision over the tubal pregnancy by a
–    Co2  laser (Paulson, 1992)
–    Argon laser (Keckstein et al; 1992)
–    Laparoscopic scissors and ablating the bleeding points with bipolar diathermy.
–    Fine diathermy knife (Lundorff, 1992)

•    The tubal pregnancy is then evacuated by suction irrigation.
•    Hemostasis of the trophpblastic bed is ensured.
•    The tubal incision is left open.


PERSISTENT ECTOPIC PREGNANCY (PEP) 
•    This is a complication of salpingotomy /  salpingostomy when residual trophoblast continues to survive because of incomplete evacuation of the ectopic pregnancy.
•    Diagnosis is made because of a raised postoperative serum HCG
•    If untreated, can cause life threatening hemorrhage
•    TREATMENT is by-
–    Reoperation and further evacuation / Salpingectomy
–    Administration of IM / oral Methtrexate in a single dose of 50 mg/m2  of body surface

SAM TREATMENT

•    Aim- trophoblastic destruction without systemic side effects
•    Technique- Injection of trophotoxic substance into the ectopic pregnancy sac or into the affected tube by-
–    Laparoscopy or
–    Ultrasonographically guided 
•    Transabdominal (Porreco, 1992)
•    Transvaginal (Feichtingar, 1987)
–    With Falloposcopic control (Kiss, 1993)

•    Trophotoxic substances used-
–    Methtrexate (Pansky, 1989)
–    Potassium Chloride (Robertson, 1987)
–    Mifiprostone (RU 486)
–    PGF2  (Limblom, 1987)
–    Hyper osmolar glucose solution
–    Actinomycin D


MEDICAL TREATMENT WITH METHOTREXATE
•    Resolution of tubal pregnancy by systemic administration of Methotrexate was first described by Tanaka et al (1982) 
•    Mostly used for early resolution of placental tissue in abdominal pregnancy. Can be used for tubal pregnancy as well
•    Mechanism of action- Interferes with the DNA synthesis by inhibiting the synthesis of pyrimidines leading to trophoblastic cell death. Auto enzymes and maternal tissues then absorb the trophoblast.
•    Ectopic pregnancy size should be < 3.5 cm.
•    Can be given IV/IM/Oral, usually along with Folinic acid
•    Recent concept is to give Methtrexate IM in a single dose of 50mg/m2  without Folinic acid.  If serum HCG does not fall to 15% with in 4-7 days, then a second dose of Methtrexate is   given and resolution confirmed by HCG estimation

Advantages –
–    Minimal Hospitalisation.Usually outdoor treatment
–    Quick recovery
–     90% success if cases are properly selected
•    Disadvantages-
–    Side effects like GI & Skin
–    Monitoring  is essential- Total blood count, LFT & serum HCG once weekly till it becomes negative




EXPECTANT TREATMENT

•    Tubal Pregnancies are known to Abort / Resolve
•    Befor the advent of salpingectomy in 1884, ectopic pregnancies were being treated expectantly with 70% mortality.
•    Today only selected cases are managed expectantly, screened and identified by high resolution ultrasound scanner and monitored by serial serum HCG assay
•    Identification criteria (Ylostalo et al , 1993)-
–    Diameter of ectopic pregnancy <4 Cm.
–    No sign of intrauterine pregnancy
–    No sign of rupture by TVS
–    No sign of acute bleeding by TVS
–    Falling level of serum HCG at 2 day intervals
•    If any deviation from the above criteria occurs, then emergency treatment is necessary.
•    Spontaneous resolution occurs in 72%,while 28% will need laparoscopic salpingostomy
•    In spontaneous resolution, it may take 4-67 days (mean 20 days) for the serum HCG to return to non pregnant level.
•    The percentage fall in serum HCG by day 7 is a better indicator than the percentage fall by day 2.
•     Warning: - Tubal pregnancies have been known to rupture even when Serum HCG levels are low.


 SUMMARY - KEY POINTS

•    Incidence of ectopic pregnancy is rising while maternal mortality from it is falling.
•    Early diagnosis is the key to less invasive treatment.
•    The choice today is Laparoscopic treatment of unruptured ectopic pregnancy.
•    The trend is towards conservative treatment.
•    Careful monitoring and proper counselling of patients is mandatory.
•    Ruptured ectopics should be unusual with compliant patients and appropriate medical care.

Labor and Delivery


Labor
►    Regular, frequent, leading to progressive cervical effacement and dilatation
►    Braxton-Hicks contractions
    May be painful and regular, but usually are not
    Do not lead to cervical change
►    Labor diagnosis usually made in retrospect.
►    Cause of labor is unknown



Latent Phase Labor
►    <4 cm dilated
►    Contractions may or may not be painful
►    Dilate very slowly
►    Can talk or laugh through contractions
►    May last days or longer
►    May be treated with sedation, hydration, ambulation, rest, or pitocin


Active Phase Labor
►    At least 4 cm dilated
►    Regular, frequent, usually painful contractions
►    Dilate at least 1.2-1.5 cm/hr
►    Are not comfortable with talking or laughing during their contractions


Progress of Labor
►    Lasts about 12-14 hours (first baby)
►    Lasts about 6-8 hours (subsequent babies)
►    Considerable variation.
►    Effacement (thinning)
►    Dilatation (opening)
►    Descent (progress through the birth canal)


Descent
►    Fetal head descends through the birth canal
►    Defined relative to the ischial spines
►    0 station = top of head at the spines (fully engaged)
►    +2 station = 2 cm past (below) the ischial spines


Cardinal Movements of Labor
►    Engagement (0 Station)
►    Descent
►    Flexion (fetal head flexed against the chest)
►    Internal rotation (fetal head rotates from transverse to anterior
►    Extension (head extends with crowning)
►    External rotation (head returns to its’ transverse orientation)
►    Expulsion (shoulders and torso of the baby are delivered)


Watch a Delivery
Placental Separation
►    Signs of separation:
    Increased bleeding
    Lengthening of the cord
    Uterus rises, becoming globular instead of discoid
    Uterus enlarges, approaching the umbilicus
►    Normally separates within a few minutes after delivery


Initial Labor Management
►    Risk assessment
►    Contractions: frequency, duration, onset
►    Membranes: Ruptured, intact
►    Status of cervix: dilatation, effacement, station
►    Position of the fetus: vertex, transverse lie, breech
►    Fetal status: fetal heart rate, EFM


Cervix
►    Dilatation: How far has the cervix opened (in cm)
►    Effacement: How thin is the cervix (in cm or %)


Status of Membranes
►    Nitrazine paper turns blue in the presence of alkaline amniotic fluid (“nitrazine positive”)
►    Vaginal secretions are nitrazine negative (yellow) because of their acidity
►    Pooling of amniotic fluid in the vaginal vault is a reliable sign



Orientation of Fetus
►    Vertex, breech or transverse lie
►    Palpate vaginally
►    Leopold’s Maneuvers


Management of Early Labor
►    Ambulation OK with intact membranes
►    If in bed, lie on one side or the other…not flat on her back
►    Check vital signs every 4 hours
►    NPO except ice chips or small sips of water


Monitor the Fetal Heart
►    During early labor, for low risk patients, note the fetal heart rate every 1-2 hours.
►    During active labor, evaluate the fetal heart every 30 minutes
►    Normal FHR is 120-160 BPM
►    Persistent tachycardia (>160) or bradycardia (<120, particularly <100) is of concern


Electronic Fetal Monitors
►    Continuously records the instantaneous fetal heart rate and uterine contractions
►    Patterns are of clinical significance.
►    Use in high-risk patients.
►    Use in low-risk patients optional


Normal Patterns
►    Normal rate
►    Short term variability (3-5 BPM)
►    Long term variability (15 BPM above baseline, lasting 10-20 seconds or longer)
►    Contractions every 2-3 minutes, lasting about 60 seconds


Tachycardia
►    >160 BPM
►    Most are not suggestive of fetal jeopardy
►    Associated with:
    Fever, Chorioamnionitis
    Maternal hypothyroidism
    Drugs (tocolytics, etc.)
    Fetal hypoxia
    Fetal anemia
    Fetal arrythmia

Bradycardia
►    Sustained <120 BPM
►    Most are caused by increased in vagal tone
►    Mild bradycardia (80-90) with retention of variability is common during 2nd stage of labor
►    <80 BPM with loss of BTBV may indicate fetal distress


Late Decelerations
►    Repetive, non-remediable slowings of the fetal heartbeat toward the end of the contraction cycle
►    Reflect utero-placental insufficiency


Early Decelerations
►    Periodic slowing of the FHR, synchronized with contractions
►    Rarely more than 20-30 BPM below the baseline
►    Innocent
►    Associated with fetal head compression


Variable Decelerations
►    Variable in onset, duration and depth
►    May occur with contractions or between them
►    Sudden onset/recovery
►    Increased vagal tone, usually due to some degree of cord compression

Severe Variable Decelerations
►    Below 60 BPM for at least 60 seconds
►    If persistent, can be threatening to fetal well-being, with progressive acidosis


Prolonged Decelerations
►    Last > 60 seconds
►    Occur in isolation
►    Associated with:
    Maternal hypotension
    Epidural
    Paracervical block
    Tetanic contractions
    Umbilical cord prolapse

Pain Relief
►    Narcotics
►    Continuous Lumbar Epidural
►    Paracervical Block
►    50/50 nitrous/oxygen
►    Psychoprophylaxis (Lamaze breathing)
►    Hypnosis


Anesthesia During Delivery
►    Local
►    Pudendal Block
►    Epidural
►    Caudal
►    Spinal
►    50/50 nitrous/oxygen


Episiotomy
►    Avoids lacerations
►    Provides more room for obstetrical maneuvers
►    Shortens the 2nd Stage Labor
►    Midline associated with greater risk of rectal lacerations, but heals faster
►    Many women don’t need them.


Clamp and Cut the Cord
►    Clamp about an inch from the baby’s abdomen
►    Use any available instruments or usable material
►    Check the cord for 3-vessels, 2 small arteries and one larger vein


Inspect the Placenta
►    Make sure it is complete
►    Look for missing pieces
►    Look for malformations
►    Look for areas of adherent blood clot