Saturday, August 17, 2019

Breast feeding in special cases

Hello Awesomites!

-HIV positive mother
-Active Pulmonary TB
-Working mothers



CONTRAINDICATION OF BREASTFEEDING :

  • HIV, HTLV-1 and 2
  • Inborn error of metabolism LIKE GALACTOSEMIA AND PHENYLKETONURIA
  • Untreated case of tuberculosis
  • Herpes lesion on mothers’ breast
  • Mother on certain medication like anti-cancer drug or radioactive isotope etc.
WITH INCREASED BURDEN OF HIV AND TB,INDIA CAN’T AFFORD TO  CONTRAINDICATE THE BREASTFEEDING.


  1. IS THERE ANY RELATION BETWEEN BREASTFEEDING AND RISK OF TRANSMISSION?
  2. DO ART HAS ANY ROLE TO DECREASE THE TRANSMISSION?


ARV INTERVENTION
RISK OF HIV TRANSMISSION FROM MOTHER TO CHILD
NO ARV                 BREASTFEEDING +
30-45%
NO ARV                 BREASTFEEDING -
20-25%
3ARVS(ART)         BREASTFEEDING +
2%
3ARVS(ART)         BREASTFEEDING -
1%

HOW TO KNOW THE HIV STATUS OF CHILDREN LESS THAN 18 MONTHS?

 
METHOD USED - DNA PCR on a DRIED BLOOD SAMPLES OF INFANT
TEST PERFORMED -

  • 6 WEEKS
  • 6 MONTHS
  • 6 WEEKS AFTER CESSATION OF BREAST FEEDING (if being EBF)
  • 18 MONTHS

PEDIATRIC COMPONENT IN PPTCT


  • DURATION OF NEVIRAPINE PROPHYLAXIS TO HIV EXPOSED INFANT SHOULD BE MINIMUM OF 6 WEEKS.


  • INITIATION OF BREAST FEEDING WITHIN AN HOUR OF DELIVERY AS THE PREFERED OPTION


  • CONTINUE BF ATLEAST FOR 1 YEAR FOR THOSE WITH HIV -VE STATUS  AND 2 YEARS FOR HIV +STATUS OF CHILDREN


  • ENSURE INITIATION OF CO TRIMOXAZOLE PROPHYLACTIC THERAPY AT 6 WEEK OF AGE



MATERNAL COMPONENT IN PPTCT
“ART TO ALL PREGNANT AND BREASTFEEDING WOMEN LIVING WITH HIV “

TARGET POPULATION
ART REGIMEN
PREGNANT AND BREAST FEEDING WOMEN WITH HIV 
BUT NOT ON ART
TDF+3TC+EFV
PREGNANT WOMEN AND BREAST FEEDING WOMEN WITH HIV AND RECIEVING ART
THE SAME ART REGIMEN MUST BE CONTINUED 
  
AFASS
 

AFASS CRIETRIA is used to decide whether a HIV positive mother can breast feed or not provided that she has not started top feed yet.
(Why? Once the mother started to top feed the child, this criteria is not used. HIV positive mother in such case should continue top feed. Because mixed kind of feed is more dangerous than top feed alone)

  • Acceptable: The mother perceives no problem in replacement feeding.
  • Feasible: The mother (or family) has adequate time, knowledge, skills, resources and support to correctly mix formula or milk and feed the infant up to 12 times in 24 hours.
  • Affordable: The mother and family, with community or health system support if necessary, can pay the cost of replacement feeding without harming the health or nutrition status of the family.
  • Sustainable: Availability of a continuous supply of all ingredients needed for safe replacement feeding for up to one year of age or longer.
  • Safe: Replacement foods are correctly and hygienically prepared and stored, and fed preferably by cup.


QUESTIONS

  1. Where do you get your drinking water?
  2.  What kind of latrine/toilet do you have?
  3.  How much money could you afford for formula each month?
    Ps: calculate the amount based on the local costs
     
  4. Do you have a refrigerator with reliable power?
     
  5. Can you prepare each feed with boiled water and clean utensils?
     
  6. How would you arrange night feeds?
     
  7. Does your family know that you are HIV positive?
     
  8. Is your family supportive of milk feeding and are they willing to help

MANAGEMENT OF BABY BORN TO MOTHER WITH TUBERCULOSIS:-


  • Continue exclusive breastfeeding till 6 months of age & thereafter as in normal population.
  • Start ATT for mother immediately. Mother will be non infective within 2 months of regular ATT


  • Preventive Chemotherapy for baby (INH 5 mg/kg/day for 6 months)


  • Use face mask while around the baby, till 2 months after starting ATT.


  • BCG Vaccine at birth.Something is better than Nothing!


  • Re- immunized with BCG after stopping Preventive Chemotherapy. 
  • (Remember, it's not only mother, Anybody (with TB) around can infect the baby with Tuberculosis!)

Is ATT drug concentration in breast milk sufficient for the baby? NO

NAME OF THE GROUP
BREAST FEEDING
BARRIER METHOD
ISOLATION
BCG VACCINATION
IAP
TO CONTINUE
COUGH HYGIENE
1.IF MOTHER ON TREATMENT -NOT REQUIRED


2.IF MOTHER HOSPITALIZED, NON-ADHERENT TO THERAPY,MDR-TB - ISOLATION REQUIRED
AT BIRTH 
OR 


EVEN WITH INH PROPHYLAXIS
DOTS
ONLY IF MOTHER IS SPUTUM NEGATIVE
FACE MASK
IF MOTHER HAS ACTIVE DISEASE,NON-COMPLIANT AND HAS RECIEVED ATT PRIOR TO DDELIVERY 
POSTPONED
OR DONE
WITH INH RESISTANT OF BCG VACCINE 
AAP
ONLY IF MOTHER IS ON ATT
FACE MASK
MDR -TB AND NON COMPLIANT
GIVE BCG IN THESE MDR TB MOTHER
WHO
TO CONTINUE
FACE MASK
MDR -TB
INH THERAPY COMPLETED THEN AFTER 2 WEEK  OF COMPLETION BCG VACCINE GIVEN 
 THE DOUBT OF WORKING MOTHERS :-

For How long can expressed breast milk is stored? 


AT ROOM TEMPERATURE 
8-10 HOURS
IN A REFRIGERATOR
24 HOURS
IN A DEEP FREEZER (-20 degree)
3 MONTHS

HAPPY STUDYING ! 
-UPASANA Y.

Friday, August 16, 2019

Lamotrigine: A depression mood stabilizer

Lamotrigine is used primarily as an anticonvulsant for the treatment of generalized and partial seizures and is effective for treating focal epilepsies in the presence or absence of secondary generalization.

Friday, August 9, 2019

Photophobia vs blepharospasm

Both have the same presentation of tight lid closure.

In dark, blepharospasm won't be completely abolished while photophobia would.

Anaesthetisation(topical) reduces greatly the blepharospasm but not photophobia.

-Sushrut

Tuesday, August 6, 2019

Definition of generalized convulsive status epilepticus

Hi everyone,

Historically, the International League Against Epilepsy (ILAE) and others defined status epilepticus as a single epileptic seizure of >30 minutes duration or a series of epileptic seizures during which function is not regained between ictal events in a 30-minute period.

However, a 30-minute definition is neither practical nor appropriate in clinical practice.

Glucagon-like peptide-1 (GLP-1) receptor agonists

Hello everyone!

Let's talk about glucagon-like peptide-1 (GLP-1) receptor agonists today!

Sunday, August 4, 2019

Tetralogy of Fallot: The Basics

Hey guys, this post highlights the important points discussed in the accompanying video.


Fuch's s in Ophthalmology

Following this are ascribed to Fuch

1. Fuch's heterochromic iridocyclitis
2. Fuch's corneal endothelial dystrophy
3. Gyrate atrophy of the choroid
4. Ciliary body adenoma

-Sushrut

Leptospirosis

Rats, rains, ricefields?
Ringing any bells?
Sewer workers coming in with jaundice and fever?
Still no?
Assam/Odisha/Kerala floods?
This spirochete called Leptospira is the culprit.
Most common species is L. interrogans and L. biflexa.
It is epidemologically important as high case fatality rate (CFR) between 5-20%
It affects 1.03 million people anually.
Endemic in states of Kerala, Tamil Nadu, Karnataka, Gujrat, Odisha and Andaman Islands.
Males suffer more than females.
More common post monsoon, natural disasters like floods and cyclones.
Transmission- water or soil contaminated by the urine of infected animals or by direct contact with infected animals such as cattle, buffalo, goat, sheep and pigs carriers of infection.
Rodents harbour leptospira in their renal tubules LIFELONG!!! and are considered reservoir hosts.
Leptospira forms biofilms for survival in renal tubules of reservoir and carrier animals.

Vascular endothelial damage is the primary lesion in leptospirosis ,after entry in the host.

CLINICAL  PRESENTATION
1. Anicteric phase- symptoms unnoticed. Sudden onset of remittent fever, chills, severe myalgia, intense headache and B/L conjunctival suffusion.
Mild proteinuria with few casts and cells in urine, cough and chest pain.
2. Icteric phase-  severe form of disease, where lepto from blood vessels trasfered to organs.
C/F- fever, myalgia, headache, conjunctival suffusion, acute renal failure-oliguria, anuria, nausea, vomiting, diarrhoea, abdominal pain, hypotension.
Elevated transaminases, leucocytes, erythrocytes in  urine, albuminuria, increases in blood urea and creatinine.

LIVER+ KIDNEY= WEIL'S DISEASE
HEPATIC- mild to severe jaundice, tender hepatomegaly, hepatic encephalopathy
RENAL-  acute tubular necrosis(ATN) , interstitial necrosis, renal failure.
RBC casts are common in urine microscopy.
PULMONARY- cough, respiratory distress, basal and mid zone opacities, hemorrhagic pneumonitis, interstitial and intra alveolar hemorrhages
CVS- shock, arrythmias
CNS-meningitis, irritability and restlessness, seizures, encephlitis, focal neurological deficits macular, maculopapular erythmatous skin irruptions
Pregnancy with leptospirosis BAD PROGNOSIS.
LAB- elevated WBC, Neutophilia, high ESR, thrombocytopenia, increased BUN and increased creatinine phosphokinase
D/D- falciparum malaria, dengue, scrub typhus, typhoid, viral hepatitis, acute encephlitis syndromes and pyelonephritis.

Diagnosis-
Dark ground microscopy, immunofluorescence, culture, histopathological staining assay.PCR
microscopic agglutination test (MAT) ELISA, IHA

Treatment and prevention:start treatment clinically
susceptible to penicillin, doxycycline, cephalosporine, tertracycline, macrolides, fluroquinolones.
DOC OPD pts. T. Doxycycline 100mg BD for 7 days, IPD severely ill- Crystalline penicilline 20Lakhs unit,6hrly. pregnant and lactating- ampicilin 500mg 6hrly
corticosteroids in gradual doses in severe hemorrhagic is considered.

prevention- rodent control, health education,personal protection, animal vaccination

Thats all folks!

Stay awesome:)

Dr. ShilPill

Thursday, August 1, 2019

No Vitamin A in Stargardt's disease

In lipofuscinoses like Stargardt's, fundus flavimaculatus, and Best's disease spectrum, Vitamin A and related compounds are avoided as the metabolites of those is what causes the disease in the first place. Usually, Vitamin A is prescribed empirically by general ophthalmologists for degenerative diseases of the retina.

-Sushrut

Wednesday, July 31, 2019

Age related macular degeneration- some facts

1. Dry AMD is the most common form, but wet AMD is responsible for 90% of the cases of visual loss.

2. Type 1 choroidal neovascular membrane is 'occult' and type 2 is 'classic'. This might be counter intuitive to remember.

3. In the genome, except for chromosome nos 7,11,13,21, and the Y chromosomes, all the other harbour genetic loci for AMD!

4. Hypermetropic eyes are at a greater risk of AMD. This, again is counterintuitive as myopic eyes are usually more prone to degenerative conditions.

5.Another, (sort of) counter intuitive fact is that 'hard' drusens do not lead to macular degeneration while 'soft' drusens precede macular degeneration.

6.Beta carotene, a treatment modality for AMD increases the risk of carcinoma of the lung in smokers as well as non smokers. Zinc causes genitourinary complications- UTIs, prostatic hyperplasia, and in women,stress incontinence. Also, zinc is ineffective in the prevention of advanced AMD. These results are from the two RCTs- AREDS 1 and 2 .

-Sushrut

Calcium channel blockers for vasospastic angina

Hey everyone!

I was reading about calcium channel blockers for vasospastic angina and it was a good refresher to know that even though they belong to the same class, they act by different mechanisms.

Dihydropyridines block slow calcium channels.

They vasodilate coronary arteries, reduce coronary resistance, increase coronary blood flow, and may enhance the development of coronary collaterals.

The vasodilatation and increase in coronary artery blood flow result from the blockade of calcium influx as well as an increase the levels of nitric oxide and bradykinin.

They can cause reflex tachycardia.

Verapamil has different physiologic effects from the dihydropyridines because of a different interaction with the calcium channels.

Verapamil is effective in angina because it decreases myocardial oxygen demand by acting as a negative inotrope and chronotrope and by lowering the systemic blood pressure.

Changes in contractility are minimal in patients without heart disease; however, verapamil can exacerbate heart failure in patients with cardiac dysfunction due to its negative inotropic activity.

Diltiazem is a potent coronary but a mild arterial vasodilator, producing improved blood flow through coronary epicardial vessels, collaterals, and normal and ischemic myocardium, as well as lowering mean arterial pressure.

That's all!

-IkaN

Inferior wall MI and Bezold-Jarisch reflex

Hello everyone!

Acute myocardial infarction (AMI), especially of the inferior left ventricular wall, is often associated with transient hypotension and sinus bradycardia.

Ever wondered... Why?

Tuesday, July 30, 2019

Kleihauer–Betke test

Kleihauer–Betke test: KB test.

1) Why do we do this test?

- To calculate Fetal RBCs in blood. This helps us to measure amount of Anti-D required to neutralize it.

2) How do we do it?

- Basically, we are going to take blood sample and add acid to it and measure red blood cells under microscope.

3) How do you differentiate Fetal and Maternal blood?

- Fetal RBCs are acid resistant. Adding acid in the preparation leads to lysis of the Maternal RBCs.

4) What are important points regarding this test that should be kept in mind while solving MCQs?

- Do not confuse it with APT test. APT is done in Alkali and it is a Qualitative test. It helps in differentiating Maternal and Fetal blood only. On the other hand, in KB test (Also know as Acid dilution test), we use Acid and we quantify Fetal blood.

- Minimum dose even after KB test is 300 microgram.

5) How do we calculate amount of Anti-D required to neutralize Fetal RBCs?

- If 20 RBCs in HPF are seen, then it means 1 ml Fetal blood is in circulation.

-‎1 ml fetal blood requires 10 microgram of Anti-D for neutralization

6) What if they don't mention "Fetal RBCs" and instead, mention "Fetal blood" in the question?

- Here is a trick. Always remember, 1 ml Fetal blood has 0.5 ml Fetal RBCs.

Applied calculations:

Q1) A Multigravida with twin pregnancy has 20 ml Fetal RBCs. How much Anti-D will be required to neutralize it?

(Take a deep breath. You don't need to worry about twin pregnancy. All the important points are already covered in above segment)

- 20 ml Fetal RBCs = 40 ml Fetal blood.
- ‎1 ml Fetal blood = 10 micrograms Anti-D

Answer = 400 micrograms Anti-D

400 micrograms is the enough amount of blood given to neutralize 40 ml fetal blood or 20 ml Fetal RBCs.

(Done easily? Perfect ! Let's level up.
I want you to go through blog once again before heading down.)

Q2) This time patient comes with same clinical presentation but with 20 ml fetal blood.

- 1 ml fetal blood = 10 micrograms of the Anti-D
- ‎20 ml Fetal blood will require 200 micrograms Anti-D.

Perfect. We calculated correctly but my question is - Will you administer 200 micrograms Anti-D to the patient showing 20 ml Fetal blood to neutralize it?

Answer is big 'NO'.

Go back to bullet (4) point 2:

Minimum amount is still 300 micrograms after KB test. So you cannot administer 200 micrograms. You have to give 300 micrograms.



I hope this blog is better than my previous blogs. Any important points you have regarding KB test, do comment in comment box

That's it

-Demotional bloke

Interesting retinal peculiarities

1. The respiratory rate of the retina is twice that of the brain.

2. The retina does not require insulin for glucose to enter the cells!

3. In the retina, glycolysis occurs despite having sufficient oxygen supply.

4. The retina is not just a sensory organ. Much of the image processing occurs at the retinal level itself.

-Sushrut

Sunday, July 28, 2019

D-lactic acidosis in short bowel syndrome

Hello everyone!

D-lactic acidosis is an unusual form of lactic acidosis.

Which patients develop D-lactic acidosis?
1. In patients with jejunoileal bypass, small bowel resection, or other causes of the short bowel syndrome.
2. Patient who receives or ingests a large amount of propylene glycol
3. Patients with diabetic ketoacidosis

In this post, I'm going to specifically talk about D-lactic acidosis in patients with small bowel syndrome.

How do patients with D-Lactic acidosis present?

Increased anion gap metabolic acidosis.
Neurologic findings of intermittent confusion, slurred speech, and ataxia.

Why does it happen in patients with small bowel syndrome?

Glucose and other carbohydrates are normally absorbed by the small bowel. If the small bowel is bypassed, removed, or diseased, then delivery of these substances to the colon increases.

Also, overgrowth of gram-positive anaerobes, such as Lactobacilli seen in small bowel syndrome contributes to lactic acidosis.

How is it metabolized?

D-lactate is not metabolized by L-lactate dehydrogenase, the enzyme that catalyzes the conversion of the physiologically occurring L-lactate into pyruvate. Thus, D-lactate is slowly metabolized in humans, accumulates in body fluids, and generates metabolic acidosis.

Diagnosis:
Laboratory studies show increased anion gap metabolic acidosis with normal plasma lactate levels, because the D-isomer is not measured by conventional laboratory assays for lactate. Diagnosis is confirmed by specifically measuring D-lactate.

Treatment:
Sodium bicarbonate if D-lactic acidosis and acidemia are severe.

Oral antimicrobial agents (such as metronidazole, neomycin, or vancomycin) can be used when D-lactic acidosis that decrease the number of D-lactate-producing organisms.
FYI: Although antimicrobials are sometimes helpful, they can occasionally precipitate D-lactic acidosis in susceptible subjects by causing an overgrowth of lactobacilli.

Low-carbohydrate diet (or the use of starch polymers rather than simple sugars) is also helpful because it diminishes carbohydrate delivery to the colon.

That's all!

-IkaN

INTERNSHIP DIARIES EPISODE 05 – Who Resides In Your Blood? (Blood Cultures)



It was a bright day. You reached the ICU ward and introduced yourself to the resident there.You got ready with cap and mask and asked to take vitals of patient.

"He developed a spiking fever, and the central venous catheter was removed on day 14 of treatment. Fever is not responding to antibiotics, Sir." said one resident to the  consultant.

"Send the blood for culture and inform me." said the consultant.

"Dr. Kesh , Can you arrange the items for sampling and fill up the laboratory forms?" the senior resident looks at you.

"Yes, Sir." Says you excited to know and expand your knowledge about blood culture.

**********************************

5.1 BLOOD CULTURES:

INDICATION FOR BLOOD CULTURE:

1.Where the possibility of septicemia or bacteremia is suggested by the presence of fever,shock or other signs and symptoms occurring in association with a known or suspected local infection such as sepsis in a surgical wound ,Osteomyelitis,peritonitis,Arthritis,Enteric fever.
2.Pyrexia of unknown origin (temperatures of >38.3°C (>101°F) on several occasions with fever of >3 weeks and failure to reach a diagnosis despite 1 week of inpatient investigation)
3.Unexplained leucocytosis or leucopenia
4.Suspected fungemia specially in Immunocompromised patients, HIV patients.

STEPS:
I)Obtain consent
II)Hand washing
III)Arranging items for sampling (MATERIALS REQUIRED)
·        70% isopropyl alcohol swabs
·         10% Povidone iodine swabs
·        dry cotton
·        Sterile gloves of suitable size
·        2 syringes (adult: 20 cc, paediatric: 5 cc)
·        2 needles (adult: 22 gauge or preferably larger butterfly or standard needle; paediatric: 25- or 23-gauge butterfly or standard needle)
·        Blood culture bottle (Aerobic and anerobic)
IV) vein selection
• Arterial vs venous blood
 • Indwelling arterial or venous lines
• Central or peripheral
V)Hand washing and Gloving
VI)Preparation of a skin
VII)Venepuncture and drawing a blood sample
VIII)Inoculating in blood culture bottle and shake the bottle
IX)Labelling, storing and documenting

• Ask the patient about allergies to iodine.
• Apply the tourniquet, select the site.
(Be careful that the ends of the tourniquet do not fall onto the puncture site, thereby contaminating it, if the tourniquet does accidentally touch the prepared puncture site, the site must be recleaned)
• Apply alcohol/acetone pad at the puncture site for 30 seconds till it dry.
• Apply the iodine swab, apply to puncture site, move the iodine in concentric circles outward. Keep it for 60 seconds (till it dry).
• Again, clean the site with alcohol/acetone and allow it to dry.
• Perform the venepuncture, following routine venepuncture procedures. Do not repalpate the site.
• If the blood culture is one of a series of samples to be drawn from a patient, the blood culture must be collected first.
• Withdraw needle from vein and insert into the top of the blood culture container.
(Other than syringe and needle, by closed system, consisting of vacuum bottle and double needle collection tube can be done.)
• Do not change the needle.
• Do not hold the container in your hand, this may result in a needle exposure.
• Do not push the blood. Mix the content. (An adequate space above broth ensures that blood is not injected under undue pressure and some air is still available for strict aerobes)
• Keep at room temperature.
• Label the blood specimen collected, following standard labelling procedures. Be sure to include the site used and the number of the specimen in the series ordered.

Blood Cultures should NOT be taken from the following sites
       Veins which are immediately proximal to an existing peripheral IV cannula.
       A femoral vein due to difficulty in skin disinfection of the site. This area poses a high risk of contamination.
       Catheter drawn blood cultures are equally likely to be truly positive (associated with sepsis), but more likely to be colonized.
(One drawn through catheter and other drawn through vein PPV of 96%)

VOLUME OF BLOOD drawn is the single most important factor influencing sensitivity
• For adult: minimum 10 ml
 • For infant and children: 1-5 ml
1-2 ml= neonate
 2-3ml= 1 month - 2year age
 3-5ml= Older children
 • 20 ml of blood obtain in sequence is more effective and sensitive (98%) specially in intermittent bacteremia.
 • Patients who have received antibiotics should give 3 separate collections of blood. Also, one or two of which on 2nd day also.

TIMING OF BLOOD CULTURE
• Before starting antimicrobial therapy
• At the time of fever peak
 • Minimum 30-60 minute interval between 2 samples except in critically ill septic patient.
 • In continous bacteremia-timing of blood culture is not important, but in intermittent bacteremia 2 or 3 culture should be spaced an hour apart.

TEST PERFORMED AFTER SAMPLE REACH TO LABORATORY
Blood to broth ratio: 1:5 only, should not be <1:5 or > 1:10
• Agitation during incubation
-  Length of incubation: • Not more than 7 days • 5 days is sufficient • >5 day-contaminants • 7 days is useful for: • Fungemia • Bacteremia due to fastidious organisms like HACEK group, brucella, legionella • For patients suspected of endocarditis who has been treated with antimicrobial before obtaining blood culture • Mycobacterial culture > 4 weeks
• Atmosphere of incubation: aerobic and anaerobic

ASK YOUR MICROBIOLOGICAL DEPARTMENT TO HELP YOU IN SELECTION OF BROTH :
• Glucose broth: useful in endocarditis
• Bile broth: In enteric fever
• Trypticase soy broth (inhibits Neisseria and S.pneumoniae)
• Brain heart infusion broth: multipurpose broth
• Thioglycolate broth: for anaerobes
• Columbia or brucella broth
• Mycobacteria: Middlebrook 7H9 with 0.05% SPS, BHI with 0.5 % polysorbate 80
• Fungus broth
Additives in broth: • Anticoagulant- bacteria are trapped in blood clot • Antimicrobial- if patient is already in antibiotics • Anticomplementry agents- to inactivates complement action • Antiphagocytic

 Type of blood culture bottle (AEROBIC AND ANAEROBIC CULTURE BOTTLE)
• Standard aerobic bottles- most common bacterial pathogens, including aerobes, facultative anaerobes and for candidemia
• Smaller bottles are used for neonates and young children
• After inoculation, bottles are incubated aerobically.

SIGNS OF BACTERIAL GROWTH:
• Macroscopically:
-Generalized turbidity
-Hemolysis
- Gas production
- Discreate colonies on the surface of the sedimented red cells
-recoverable bacterial growth may occur before turbidity is evident.
Subculture from bottles as a routine
  • For subculture:
- Subcuture should be done at least once during the first day after 5-6 hours and at interval thereafter which should be at least twice during first 2-3 days.
Gram stain:  Should be made and examined at the subculture stage. Any positive finding should be reported at once to clinician as the morphological type of organism may guide the physician to start antibiotic.
Quantitative counts of bacteria in blood: Inoculate 1 ml amounts of blood into several tubes of melted agar and make pore plates either directly from patients. Another method is treat the patient sample with lytic agent. Then lysed sample is centrifuged and harvested organism cultured directly on a suitable solid medium to allow identification and to give a semi-quantitative indication of its presence in blood. (When monitoring colonization associated with a prosthesis or catheter) 

INTERPRETATION OF POSITIVE BLOOD CULTURE REPORT:
1. Whether true or contaminant (ASEPSIS, ASSES RISK FACTOR PRESENT IN PATIENT)
2.FIND THE SOURCE
3.DETERMINE THE NEED FOR TREATMENT (whether patient is toxic and in shock)
4.ADDRESS UNDERLYING INFECTIOUS FOCUS
5.LOOK FOR PATHOGEN SPECIFIC FACTORS DURING ANTIBIOTIC TREATMENT (Toxins that are produced)
6.HELPS IN IDENTIFYING OTHER RISK FACTOR WITH INFECTION (The identification of S.bovis organism also prompted the ultimate identification of colonic carcinoma, which is an underlying risk factor for S. bovis bacteremia)
7.LOOK FOR REASON OF IMMUNOCOMPROMISED STATE (Rule out malignancy or HIV as bactremia may be a result of oppurtunistic infection)

Therefore,clinical examination is of utmost important. As positive blood culture is not a disease in itself. It may be a result of underlying disease or part of complication.
After starting treatment, document the blood culture clearance duration.

SOME DEFINITIONS:

Bacteremia – presence of bacteria in blood stream.Some conditions have a period of bacteremia as part of the disease process (ex. Meningitis, endocarditis)

Septicemia – bacteremia plus clinical signs and symptoms of bacterial invasion and toxin production

Transient bacteremia lasts for minutes or a few hours and most frequently occurs after manipulation of nonsterile body sites—for example, during dental procedures; after gastrointestinal biopsy; after percutaneous catheterization of the vascular system, bladder, or common bile duct; and after surgical debridement or drainage—that is, after procedures involving contaminated or colonized skin and/or mucosal surfaces are performed and also at the onset of acute bacterial infections.

Intermittent bacteremia is defined as bacteremia due to the same microorganism that is detected intermittently in the same patient because of a cycle of clearance and recurrence. Intermittent bacteremia is often associated with undrained closed-space infections, such as intra-abdominal or soft-tissue abscesses, and may also occur in patients with liver abscesses, cholangitis, and focal infections, including pneumonia, osteomyelitis, and spondylodiscitis. 

Persistent bacteremia is a characteristic of infective endocarditis (IE) and other intravascular infections, such as vascular-graft infection, a mycotic aneurysm, or an infected thrombus. Persistent bacteremia also occurs during the early stages of systemic bacterial infections, such as brucellosis and typhoid fever.

********************************
After labelling the sample, storing and documentation, you went to ICU again. Taking vitals and documenting it in files. Feeling happy to learn about blood culture. 

*******************************

HAPPY STUDYING !
UPASANA Y. AND JAY

Friday, July 26, 2019

Fas- fas ligand interactions and uveitis

-Fas ligand/ FasL/ CD95 ligand is a type 2 membrane protein belonging to the TNF superfamily and is found on lymphocytes.

-In the eye, it is expressed on Iris and corneal endothelial cells.

-In the rest of the body, it is expressed on the thymus, testes, and the brain.

-Liver and intestines express this only in periods of severe inflammatory process.

- Apoptosis of the T lymphocytes can be triggered by FasL. Loss of this mechanism is touted to be one of the causes of uveitis.

Mechanism by which it acts is believed to be the selective apoptosis of cells producing TNF or by IL2 activation of lymphocytes.

-Sushrut

Effector blockade in the eye.

This is a mechanism by which the eye wards off the secondary effector phase of the immune response arc.
Thus, the cell mediated immunity appears to function less effectively in the uvea compared to the rest of the body.
Possible mechanisms include-

1. Immunomodulatory cytokines produced by the ocular tissues.

2. Immunomodulatory neuropeptides produced by ocular nerves

3. Functionally unique APCs.

4. Compliment inhibitors

..and some other factors.

-Sushrut

Choroid and fungi

The large spaces of choroid act as a sort of trap to organisms, especially fungi. Therefore most fungal lessons of the posterior segment begin as choroiditis.

Wednesday, July 24, 2019

Relative risk of invasive breast carcinoma based on histological examination

Hello Awesomites!

I was going through some questions on Breast cancer. Found this piece of information.

Based on histological examination of benign breast tissue, we can assess the relative risk of invasive breast carcinoma.
Why do we want to assess this? In some studies it has been found that histologic features, the age at biopsy, and the degree of family history are major determinants of the risk of breast cancer after the diagnosis of benign breast disease. 

1. Findings suggestive of No increased risk
-Adenosis (sclerosing or fibroid)
-Cystic (macro & /micro)
-Duct ectasia
-Fibrosis
-Fibroadenoma
-hyperplasia
-Mastitis
-Squamous metaplasia
-Periductal Mastitis

2. Findings suggestive of slightly increased risk (1.5 to 2 times)
-Hyperplasia, moderate or florid, solid or papillary
-papilloma with fibrovascular core

3. Finding suggestive of moderately increased risk (5 times)
-Atypical hyperplasia, ductal or lobular

4. Insufficient data to assign a risk
-solitary papilloma of lactiferous sinus
-Radical scar Lesion

Happy Studying!
Upasana Y. :)

Chronic thromboembolic pulmonary hypertension (CTEPH)

Hello everyone,

We will be talking about CTEPH today.

Tuesday, July 23, 2019

Calot's triangle vs Cholecystohepatic triangle

Hello Awesomites!

I would like to highlight difference between these two terms. It is confusing.

1.Cholecystohepatic triangle:

Medial boundary- Common hepatic duct
Inferior boundary- Cystic duct
Superior boundary- Inferior edge of liver

2. Calot's triangle:

Medial boundary- Common hepatic duct
Inferior boundary- Cystic duct
Superior boundary- Cystic artery

Happy Studying!
Upasana Y. :)

Efferent optic nerve fibres

It's interesting to note that the optic nerve, which is considered to be a purely sensory nerve has some efferent fibres, that is, fibres from the brain to the optic disc. The presumed role of these fibres is in dreams, where the brain sends impulses to the retina, image is generated and it is carried back to the brain via the afferent fibres.

-Sushrut

CEAP classification of Chronic venous insufficiency

Hello Awesomites!

The classification and staging of chronic venous insufficiency (clinical severity) can be measured by a scoring system called clinical manifestations, etiological factors, anatomical distribution, and pathophysiological conditions.

Happy Studying!
Upasana Y. :)


Monday, July 22, 2019

Anterior chamber associated immune deviation

Some specific antigens when placed in the anterior chamber of the eye result in a suppression of cell mediated immunity, with a normal humoral component.

There is something known as the ' oculo splenic axis' , whereby the antigens travel via the trabecular meshwork and reach the spleen. In the spleen, they secrete MIP 2 which attracts the NK cells. The NK cells in turn secrete IL10 and TGF beta. The T cells in this environment become regulatory cells and suppress the cell mediated immunity. Production of IL2 is suppressed.

The eye is an immuno privileged organ, as it needs to be structurally maintained pristine to preserve it's light carrying capability. ACAID is a mechanism by which Nature attempts to limit unwanted inflammatory responses in the anterior chamber.

It has implications in intraocular tumors, autoimmune, and infectious immune responses.

-Sushrut

PS- The failure of ACAID in the mechanism of lens induced uveitis still remains unexplained!

ACCF/AHA versus ESC guidelines: Pharmacologic therapies for management of HFrEF

Hello everyone!

This video is based on the ACC/AHA guidelines from 2013 in addition to ACC/AHA 2017 update vs ESC guidelines from 2016. I recommend watching at 2x speed because I talk too slow :P


 

Saturday, July 20, 2019

What it takes to be a compassionate physician

Hello everyone!

I participated in the Daniels Family Foundation Scholarship in honor of an honorable physician at my program.  The requirement to participate was to submit a brief (500 words or less) essay that describes how you have demonstrated what it takes to be a compassionate physician dedicated to the practice of general internal medicine.

If possible, I want you to write an essay too. Please email them to me (medicowesome@gmail.com). I would love to hear your experiences (and maybe even publish them on Medicowesome if you'd like)

Let me go first and share my essay with you:

Friday, July 19, 2019

Authors diary: Are you ready for solo practice?

"Are you ready for solo practice?"

My father read out the topic from a WhatsApp forward he had received.

I was drinking tea, with all the absent-mindedness of a resident who barely has the luxury to sit down and have said cup of tea.

I stared at my father aghast, wondering where this daunting question sprung from, till he elaborated that it was the topic of an essay competition.

As I read through the message myself I corrected him, "That’s not what it says! It's asking whether you're adequately trained for solo practice in the future."

"Your future is just a couple of years away. Will you be ready by then?" he asked.

"I don’t know about ready, but I’m sure I’ll be adequately trained," I answered.

He nodded and after a beat, leaned in and asked,
"But have you really thought about it yet?" ((And what makes you so sure? Have you really thought about it yet?))

That got me thinking indeed.

As a year old paediatrician, the most important lesson I learnt was how much there was to learn. My days were spent working with any time off work spent catching up on missed sleep. I felt like I whizzed through my first year, barely retaining any of the knowledge I was expected to glean as an intern. Being a houseman had felt like operating at spinal level, for the lack of there being a synaptic level
any lower than that. Perhaps I wasn't ready at all.

My face seemed to betray my thoughts as my father interrupted them. "Instead of lamenting over what you haven’t learnt," he asked kindly, as if reading my thoughts, "Why don’t you try and think about how much you have?"

Convinced that I had learnt nothing of value anyway, I decided to humour him nevertheless. I spoke about  my housemanship month by month, about what each sick child and each hopeful parent had taught me. A resident doctor in a busy municipal hospital barely gets time for their own basic life needs like food, sleep, or even a bath (and needless to say, sleep always takes priority!). Most of what we learn is on the go. Nobody gets enough time to go back and read about the cases we've seen in the ward. Thankfully the vast number of cases and immense workload ensures that we at least know how to manage basic ailments that a child presents with.
However amidst putting orders, histories, and ensuring investigations for so many patients, we forget to learn about the little things - how to allay a parent's concerns about their child, how important the so called 'cosmetic' part of our practice is. Of course, all these concerns are still things that can be worked on if one can put their heart into it.
And yet, are we being adequately trained to do this for future solo practice? The answer, shockingly, is a resounding no.

Add to this, we're barely trained to make decisions by ourselves, especially when there are so many seniors waiting to teach us, guide us, and by extension, take responsibility for our actions. How is one supposed to adjust to suddenly being so independent?

In a tertiary care setting, we are used to sending out references left, right, and centre. We fail to learn the basics of anything that would result in us putting even one toe out of our own speciality and instead rely on the services of others, who are just a single written call away. It's very obvious that this is not going to be the case when one starts practising by oneself.

Another important thing that nobody teaches you in residency is how to ask for remuneration for our services. Being employees of the state or the corporation, we are used to working endlessly for a fixed salary being ddeposited in our accounts each month. As a result, we fail to realise our worth in monetary terms, there being a certain amount of guilt with each patient we charge. Maybe this is something we realise only after getting into private practice, where taking care of every patient is translated into putting food on our own plate. At this stage in life, while I hope I wouldn't underestimate and thus undercharge for my abilities, I really don't know what that would be like be like.

So, coming back to the question that started it all - no, I am not adequately trained for future solo practice. And no, I am not ready for it either. But two years down the line, I have hope for the former statement. And as for the latter? Well, I believe that at least that "I'm not ready." will transform into" I'm not ready...yet. But I'm willing to stick around till the day I am."

Written by Aditi

Wednesday, July 17, 2019

ACEI and ARBs in congestive heart failure

Hey everyone!

Today, I will be talking about ACEI and ARBs in congestive heart failure (based on ACC and ECS guidelines).

Here are a few points on what the guidelines say:

Friday, July 5, 2019

EPISODE 04 - INTERNSHIP DIARIES (What will I do with your blood? -Vials and sampling)


- By Upasana and Jay

It has been a tired day at the hospital. You are almost at the end of your day of duty when your senior resident asks you,

“Dr Kesh, can you please prepare the Laboratory forms, sign them for me and then, submit these blood samples to the Main laboratory?

“Yes sir!” You pressure a smile and look at the blood samples and the empty Laboratory request forms needing your signature and your gleaming new stamp with your licence number.

You sit down to prepare the blood samples.