OptiCard : fundoscope to use with cellphone camera

visit: www.tlabs.pk

Opticard is a fundoscope to use with cell phone camera.
This fundoscope works with and without cell phone !

Specifications:
SMD type LED White Light Source
3 Volt Button Cell CR2032 (Non-Rechargeable) (Replaceable)
ON/OFF Switch with expected 10,000 Cycles Life
Fiber Glass Light Weight Card with Imprint Lamination Printing that practically never Fades.
For details of specification regarding research purposes contact TLABS (contact@tlabs.pk)

User Instructions

LED turns ON and OFF with the button on OptiCard. LED is attached to the edge of the card . Below LED, there is an aperture for direct fundoscopy. OptiCard may be used with the cell phone camera or retinal examination may be done with naked eye.

As with the use of any other diagnostic instrument, the liability of usage of this device and patients’ safety remains the responsibility of physician.

Technique to use with naked eye:

As the button is moved Up LED turns ON. Patient’s pupil (dilated already with a mydriatic drug) is examined through the aperture of the OptiCard. From a distance of half meter(or closer) red reflex may be seen. Bring the card closer to eye till retinal vessels are visualized and follow them converging to the optic disc. (Fundus is visualized much easily with OptiCard than with traditional direct ophthalmoscope, as the distance between aperture-lightsource-observer’s eye is negligibly small(2mm) as compared to traditional Direct Opthalmoscope where this distance is (>10mm) and hence slight rotation of hand causes light rays to misalign with observer’s eye.)

Technique to use with a cell phone :

To view fundus through a cell phone the upper border of the card (with LED on its edge) is placed close to the cell phone camera aligning it to the center of the camera lens. OptiCard is turned-ON and Camera is turned on in the cell phone and by seeing on LCD , LED is adjusted such that it is just visible through the cell phone LCD (see video at www.tlabs.pk). The card may then be secured on the cell phone using sticking tape. Turn-OFF OptiCard. Focus the phone camera to some distant object about 6 feet away. Then turn-ON OptiCard ,and see through patients pupil. (Do not yet zoom) Once fundus/retina is visualized properly, then you can zoom. To use card with a zoomed camera ,it needs good practice. From half a meter distance a dilated pupil is visualized that may show a red reflex on Phone LCD.  Cell phone camera is brought closer to the eye, about an inch away from it and retinal vessels get visualized which may be followed towards the center to visualize the disc. Video or still images may be taken . 

DO NOT LET CONTACT with eye happen.

If the inbuilt camera software of the phone allows ‘manual focus’ , sharpest images may be taken in myopic or hypermetropic patients.

With practice , fundus and retina may be explored through undilated pupils also.

If the OptiCard is attached to silicone cover of cellphone , the cover may be simply detached from the phone , and attached again once needed .

OptiCard attached to cellphone by pieces of sticking tape   
      

Method to Attach to Cellphone






WARNINGS :

1. Maintain safe distance with  patient's eye. Do not make contact with the eye of patient. Do not examine for more than 45 seconds in a single go , to give rest to patient’s eye.
2. The device may be kept in wallet ensuring that no contact with liquids comes across. If it comes in contact with water, immediately remove the cell from OptiCard and let it dry.
3.This gadget is not a TOY. It has small parts. Keep it out of reach of children.
4. If any component  of OptiCard is detached or loosely attached to the piece, please do not use the card , as it might cause trauma to patient’s eye. You may contact us to assist you in repair. We’ll respond back in time.
5. Do not recharge the cell.
6. If the device comes in contact with liquids, remove the cell, and let the device air dry . The cell may then be replaced back.

Designed, Invented, Made in Pakistan.

Whenever you need assistance with the Card that you have purchased, there is a web-link on card,
simply go there, and Contact us ! We shall respond positively, always.

Your suggestions are welcomed.
Contact at :

contact@tlabs.pk

Turner syndrome - summary

EPI Schedule as per 2017 : Pakistan :: Vaccination Schedule

EPI Schedule as per 2017

Birth BCG   OPV-0    HEP-B __________________________
6 weeks  OPV-1    Penta-1   PCV-10-1    Rota-1 ______________
10 weeks   OPV-2    Penta-2   PCV-10-2   Rota-2_______________

14 weeks    OPV-3    Penta-3   PCV-10-3   IPV_________________

9 months   Measles-1____________

15months   Measles-2____________

(age yet to be decided by officials) DPT Booster__________

Any Other____________

CYSTIC FIBROSIS : summarized

CYSTIC FIBROSIS

DR Sadia Hayat

Cystic fibrosis is an inherited autosomal recessive multisystem disorder of children and adults due to primary defect in CFTR protein encoded by CF gene .F508del mutation is most common.

PATHOGENSIS :

Due to loss of fuction of  CFTR  leads to decreased secretion of chloride and increased reabsorption of sodium and water across epithelial cells

§  RESPIRATORY TRACT : due to defective chloride secretion and excess  reabsorption of sodium and water .Failure to clear mucous secretions , paucity of water in mucous secretions, an elevated salt content of sweat and other secretions .Insufficient water on airway surface to hydrate secretions .dessicated secretions become more viscid and elastic that are harder to clear by mucociliary and other mechanisms .secretions are retained and obstruct airways (first of all bronchioles)

§  GASTROINTESTINAL TRACT , PANCREAS AND LIVER

§  IN 85 % pts pancreatic insufficiency occurs which arisis from reduced bicarbonate secretion ( disturbing optimal ph for pancreatic enzymes),reduction of water content of secretions and plugging of ductules and pancreatic acini .Pancreatitis may occur .

§  In gut defective CFTR leads to reduced chloride and water secretion causes meconium ileus at birth and distal intestinal obstruction syndrome in later life

§  In liver there is increased biliary viscosity and plugging of biliary ductules ,can cause obstructive cirrhosis , portal hypertension and hypersplenism .gallstones and cholecystitis are more common in cystic fibrosis

§  SWEAT DUCTS : failure of chloride and sodium reabsorption from the sweat ducts leading to high sweat salt content

§  VAS DEFERENS : males are azoospermic because of agenesis of vas deferens ,isolated congenital bilateral absence of vas deferens (CBAVD).

CLINICAL FEATURES:

§  Respiratory tract :chronic or recurrent cough ,recurrent lower respiratory tract infections , recurrent wheezing ,recurrent sinusitis ,nasal polyps

§  Gastrointestinal ,pancreatic and hepatobiliary tracts :

§  neonatal :CF may present with intestinal obstruction at birth due to meconium ileus(7-10% pts ), passage of meconium may be delayed (due to meconium  plug),there may be prolonged cholestatic jaundice

§  infants and children :failure to thrive ,flatulence, recurrent abdominal pain and abdominal distension .Malabsorption: fat accompanied by steatorrhea(frequent ,foul smelling ,bulky stools).intussception and rectal prolapse may occur

EXAMINATION:low weight ,anemia, short stature,dry skin (vitamin A deficiency) skin rash (zinc deficiency )  ,abdominal distension , rhinitis, sinusitis and nasal polyps, clubbing, cyanosis, increased AP diameter of chest ,cough, tachypnea and recession ,wheezes or crackles on auscultation ,delayed puberty.

INVESTIGATIONS :

SWEAT CHLORIDE TEST

First line diagnostic test in suspected CF . quanatitaive pilocarpine iontophoresis test is performed. Minimum of 100 mg of sweat should be collected onto filter paper for estimaton of sodium and chloride .

·         Negative (normal) test : Cl<40 mmol/ l

·         Borderline (suggestive) :Cl 40-60 mmol/l

·         Positive (supportive ) Cl >60 mmol/l

·         GENOTYPING (DNA Analysis . CFTR analysis for F508del mutations .negative result reduces likelihood of CF but doesnot exclude it .

·          

·         CBC (anemia, Raised TLC ) ESR/CRP, Blood Culture,

·         Stool Examination for fat globules.

·         Chest X ray :hyperinflation and bronchial thickening and plugging and ring shadows suggesting bronchiectasis (first in upper lobes ) . nodular densities , patchy atelectasis ,prominent hilar lymph nodes .in advanced disease cyst formation, extensive bronchiectasis , dilated pulmonary artery segments , and segmental or lobar atelectasis apparent with advanced disease

·         Microbiology : sputum culture/ cough swab. Common bacterial pathogens are staphylococcus aureus , Pseudomonas aeruginosa , klebsiella pneumonia , Burkholderia cepacia ,and hemophilus influenza

·         CT chest : detects and localizes thickening of bronchial airway walls , mucous plugging ,focal hyperinflation and early bronchiectasis .

TREATMENT :

Main aim is to prevent progression of lung disease ,maintain adequate nutrition ,monitor for and treat complications and provide psychological report Initial efforts after diagnosis should be intensive and shouldinclude baseline assessment, initiation of treatment, clearing ofpulmonary involvement, and education of the patient and parents.Follow-up evaluations are scheduled every 1-3 mo, depending onthe age at diagnosis,

RESPIRATORY:

i)        PHYSIOTHERAPY: twice daily physiotherapy comprising postural drainage and percussion in infants and children and independent airway clearance devices with deep breathing exercises in older children

ii)       

iii)    ANTIBIOTICS: Protection against exposure to methicillin-resistant S.aureus, P. aeruginosa, B. cepacia, and other resistant gramnegative organisms is essential,Indications for oral antibiotic therapy in a patient with CF include the presence of respiratory tract symptoms and identifcation of pathogenic organisms in respiratory tract cultures.

Oral/
IV antibiotics/

inhaled antibiotics may be given.
Empirical therapy includes Azithromycin , Erythromycin .

Staphylococcus aureus :Vancomycin ,Linezolid ,Cephalexin ,Clindamycin Amoxicillin-clavulanate

Haemophilus infuenzae; Amoxicillin

Pseudomonas aeruginosa :Ciprofoxacin

Burkholderia cepacia ;Trimethoprim-sulfamethoxazole

>>Inhaled Aztreonam and tobramycin may be given.

iv)    Pancreatic Enzyme Replacement

v)      Vitamin ADEK and Calcium /Zinc Supplementation

vi)    Keep on 3 monthly followup. Assess growth parameters and asses for infections.

COMPLICATIONS OF CYSTIC FIBROSIS:

Anemia
Short stature
Infertility

Delayed puberty
Edema-hypoproteinemia

RESPIRATORY

Bronchiectasis, bronchitis, bronchiolitis, pneumonia

Atelectasis

Hemoptysis

Pneumothorax

Nasal polyps

Sinusitis

Reactive airway disease

Cor pulmonale

Respiratory failure

Mucoid impaction of the bronchi

Allergic bronchopulmonary aspergillosis

GASTROINTESTINAL

Meconium ileus, meconium plug (neonate)

Meconium peritonitis (neonate)

Rectal prolapse

Pancreatitis

Biliary cirrhosis (portal hypertension: esophageal varices, hypersplenism)

Neonatal obstructive jaundice

Hepatic steatosis

Gastroesophageal reflux

Cholelithiasis

Growth failure (malabsorption)

Vitamin def ciency states (vitamins A, K, E, D)

Insulin deficiency, symptomatic hyperglycemia, diabetes

HYPERTENSION in children : summarized

HYPERTENSION

Dr Nimrah Shehzadi

Defined as

           "Systolic and diastolic blood pressure that is > or =95th percentile  for age,sex and height on atleast 3 readings" , or systolic blood pressure of 130 mmHg in any child taken thrice.

Prehypertension :

        "Systolic or diastolic BP that are >90th percentile but <95th percentile"

Children to be evaluated :                                                                       

Every child >3 yr old

Child <3yr of age with the following risk risk factor: Hx

      prematurity

      Congenital heart disease

      Renal disease

      Solid organ transplant

      Cancer

      Drugs raising bp

       Neurofibromatosis

       Tuberous sclerosis

       Raised intracranial pressure

Etiology :

Renal abnormalities ( chronic glomerulonephritis,reflux obstuctive nephropathy,hemolytic uremic syndrome,polycystic or dysplastic renal diseases )

Vascular (coarctation of aorta ,renal artery stenosis,umbilical artery catherization,neurofibrosmatosis,renal vein thrombosis,vasculitis,

Endocrine (hyperthyroidism ,hyperparathyroidism,CAH,cushing syndrome,primary aldosteronism)

CNS (raised intracranial pressure due to intracranial mass,hemorrhage,brain injury)

Clinical manifestations :

Asymptomatic

Headache

vomiting

Dizziness

Epistaxis

Anorexia

Visual changes

Seizures

Hypertensive encephalopathy(headache,vomiting, temperature elevation,visual disturbances,ataxia,depressed level of consciousness,CT abnormalities,seizures)

Malignant hypertension (cardiac failue,pulmonary edema,renal dysfunction,Fits)

Hypertensive crisis : decreased vision(retinal hemorrhage)papilledema, encephalopathy(headache,seizures, depressed level of consciousness),heart failure,accelerated deterioration of renal function

Investigations:

Urine analysis/culture

S/E (sodium,potassium, phosphate,calcium)

Blood urea and serum Creatinine

Abdominal USG(renal )

Fasting BSL and lipid profile

Echocardiography(LVH,coarctation of aorta)

Total cholesterol and HDL, LDL  levels

Abdominal angiography (vascular lesions of renal artery)

Measurement of VMA in 24 hours urine

CT brain may be indicated.

Prevention: by avoidance of

Obesity

Elevated serum cholesterol levels

High dietary sodium intake

Sedentary lifestyle

Alcohol and tobacco use

TREATMENT

Non-Pharmacologic: Aerobic exercise, salt restriction,weight loss.

Pharmacologic treatment: it is indicated when there is target organ damage, diabetes mellitus , and persisten hypertension despite non-pharmacologic measures.

A single drug or a combination of two or more drugs can be used depending upon the situation, commonly used drugs are as follows,

ACE inhibitors (captopril)                                          0.3mg-0.5mg/kg/dose x tds

     

B-Receptor blocker (propranolol)                               0.025-0.1mg/kg/day x tds

Calcium Channel Blockers (nifedipine)                     0.2-0.5mg/kg/day xbd or qid

Diuretic  (furosemide)                                                                 0.5-2mg/kg/dose every 4-6 hourly

Vasodilators            

Hydralazine,                                                   0.25mg/kg/day

Nitropruside                                                    0.5-10 g/kg/min 1/v infusion

Management of hypertensive crises

The blood pressure should be reduced 1/3rd of total planned reduction during Ist 6 hour and remaining over 48-72 hours.

Give i/v hydralazine :
0.1 mg/kg/dose IV as infusion over 20 mins ( may need to be added 4 Hrly or 6 hrly )

Monitor B.P before giving the drug.
Consult seniors for further management.

Myocarditis in children : summarized

Myocarditis

Dr Anum Arif

Acute or chronic inflammation of myocardium characterized by inflammatory cell infiltrates, myocyte necrosis or degeneration.

Causes:

i.                    Infections:

Viral infections	Bacterial	Fungal	Protozoal	Parasitic
Adenovirus Parvovirus Ebstein barr virus Parechovirus Influenza virus Cytomegalovirus Hepatitis c virus	Diphtheria Mycoplasma pneumonia Mycobacteria Streptococcus species	Aspergillus Candida Histoplasma	Toxoplasma gondi Trypanosoma cruzi Babesia	Schistosomiasis

ii.                   Immune mediated:

Ø  Churg strauss syndrome

Ø  Ibd

Ø  Sle

Ø  Kawasaki disease

Ø  Takayasu arteritis

Ø  Celiac

iii.                 Drugs:

Ø  Sulphonamides

Ø  Cephalosporin

Ø  Diuretics

Ø  Dobutamine

Ø  Tricyclic antidepressants

iv.                 Toxic:

Ø  Snake bite

Ø  Scorpion bite

Ø  Spider bite

Ø  Ethanol

PATHOPHYSIOLOGY;

Ø  Acute deterioration: myocardial inflammation, injury, necrosis leading to cardiac enlargement systolic dysfunction and ccf ( shock, atrial / ventricular arrhythmia)

Ø  Chronic: myocarditis may become chronic with persistence of viral nucleic acid in myocardium.

CLINICAL FEATUES:
Severe respiratory distress, central/peripheral cyanosis may be there ,
cold peripheries , pallor due to circulatory failure, dehydration due to reduced intake , grunting, head nodding, nasal flaring, suprasternal,intercostal,subcostal,substernal recessions may be there.
Pulses may be good volume but later low volume or absent pulses.
Capillary refill time may be prolonged(>3 Sec)
B.P may be recordable initially but later hypotension or BP not recordable.
Altered Sensorium, or irritability due to decreased cerebral perfusion.

tachypnea,tachycardia, hyperdynamic precordium, muffled heart sounds , gallop rhythm, apical systolic murmur. Hepatomegaly due to congestive cardiac failure, peripheral edema and rales or basal crepitation may occur due to cardiac  failure.

Differential Diagnosis:
Carnitine deficiency
DCM
Hereditary mitochondrial defects
Anomalies of coronary arteries.

Diagnosis:

Ø  Ecg: lOW VOLTAGE ECG  i-e QRS complexes (QRS  amplitude of less then 5 mm in 3 consecutive limb leads and/or less then 10 mm in precordial leads.

Ø  nonspecific st and t wave changes.

Ø  Chest xray: cardiomegaly (ratio of maximum horizontal thoracic diameter and maximum cardiac diameter more then 0.5., pulmonary vascular markings, pleural effusion.

Ø  Cardiac MRI: standard imaging modality.

Treatment:

            Admit the patient.

o   Keep Cleared Airway,

               Prop up to 45 degrees

               Oxygen inhalation via NG in nostril with continuous sp02 monitoring

                Check for adequate/B/L comparable chest rise

o   Maintain I/V line
Monitor :
PR, RR, BP, CRT, Temp, BSL, Urine Output,
Attach spO2 monitor,
Attach Chest electrodes for continuous ECG monitoring.

Restricted maintenance fluids 70%  ( 5%DW + N/2 e 2ccKCl/100ml)
For inotropic support: dobutamine, dopamine, adrenaline infusion or  milrinone(50mcg/kg iv over 10-60 min followed by 0.25-0.75mcg/kg per min iv  can be used) . Consult seniors regarding choice of inotropic support .
Milrinone has the same effects as that of dobutamine , but since it acts through inhibition of Phosphodiesterase, it reduces the myocardial oxygen demand and hence reduces the mortality as compared to dobutamine.

Ø  Diuretics to reduce cardiac pre load.

                Frusemide 1mg per kg per dose X BD (after recording BP)

Ø  Immunomodulation : Intravenous immunoglobins may be given
Inflammatory dose Dexamethasone(steroids) : 1mg/kg/day has a controversial role in acute phase.
Antivirals do not have any proven role.

Ø  If arrhythmias occur, patient may need Pharmacologic or Electric cardioversion.

Ø  Mechanical ventilation may be indicated during the course of disease.