Saturday, 7 November 2015

Maternal weight gain

Cemak Asma: Maternal weight gain in pregnancy (normal bmi):
-1.6kg total in 1st trimester
-0.45kg/week in 2nd trimester
-0.4kg/week in 3rd trimester


Friday, 6 November 2015

Cystoscopy

Maryam: Indication of cystoscopy:
1) Hematuria
2) Recurrent UTI
3) Sterile pyuria
4) Short history of irritative symptoms
5) Suspected bladder abnormality (eg. Diverticulum, stones, fistula)
6) Assesment of bladder neck

Dr Shaiful Ehsan: Cystoscopy examination in relation to PP: suspected infiltration into bladder, clinical haematuria or persistent microscopic haematuria with PP.....

Traube's space

5. Traube's space
Traube's space:

Traube's space is a space defined superiorly by the 6th rib, laterally by mid axillary line and inferiorly by the left costal margin.

Normally, this space is resonant to percussion. In the presence of pleural effusion and splenomegaly, it becomes dull.

With the patient lying supine, abduct the patient's left arm slightly, ask the patient to breathe normally and percuss across the space from its medial to lateral margins at a couple of levels. The note should remain resonant unless the spleen is enlarged.

Gullain Barre syndrome

4. Gullain Barre syndrome
Guillain-Barre (gee-YAH-buh-RAY) syndrome is a rare disorder in which your body's immune system attacks your nerves. Weakness and tingling in your extremities are usually the first symptoms.

These sensations can quickly spread, eventually paralyzing your whole body. In its most severe form Guillain-Barre syndrome is a medical emergency. Most people with the condition must be hospitalized to receive treatment.

The exact cause of Guillain-Barre syndrome is unknown. But it is often preceded by an infectious illness such as a respiratory infection or the stomach flu.

There's no known cure for Guillain-Barre syndrome, but several treatments can ease symptoms and reduce the duration of the illness. Most people recover from Guillain-Barre syndrome, though some may experience lingering effects from it, such as weakness, numbness or fatigue.
Signs and symptoms of Guillain-Barre syndrome may include:

Prickling, "pins and needles" sensations in your fingers, toes, ankles or wrists
Weakness in your legs that spreads to your upper body
Unsteady walking or inability to walk or climb stairs
Difficulty with eye or facial movements, including speaking, chewing or swallowing
Severe pain that may feel achy or cramp-like and may be worse at night
Difficulty with bladder control or bowel function
Rapid heart rate
Low or high blood pressure
Difficulty breathing
People with Guillain-Barre syndrome usually experience their most significant weakness within two to four weeks after symptoms begin. Recovery usually begins two to four weeks after weakness plateaus.
The exact cause of Guillain-Barre syndrome isn't known. The disorder usually appears days or weeks after a respiratory or digestive tract infection. Rarely, recent surgery or immunization can trigger Guillain-Barre syndrome.

In Guillain-Barre syndrome, your immune system — which usually attacks only invading organisms — begins attacking the nerves. In AIDP, the most common form of Guillain-Barre syndrome in the U.S., the nerves' protective covering (myelin sheath) is damaged. The damage prevents nerves from transmitting signals to your brain, causing weakness, numbness or paralysis.

Wernicke's encephalopathy

3. Wernicke's encephalopathy
The three components of the classic triad of WE are encephalopathy, ataxic gait, and some variant of oculomotor dysfunction. However, a complicating factor of WE identification is that its presentation may not be associated with the classical clinical triad in up to 90% of patients.

Consideration for WE should be given to patients with any evidence of long-term alcohol abuse or malnutrition and any of the following: acute confusion, ataxia, ophthalmoplegia, memory disturbance, hypothermia with hypotension, and delirium tremens.

A high proportion of patients with acute WE who survive develop WKS, characterized by potentially irreversible retrograde amnesia (inability to recall information) and anterograde amnesia (inability to assimilate new information), with varying degrees of other cognitive deficits.

Consider WE when any patient with long-term malnutrition presents with confusion or altered metal status. Significant overlap exists between WE and Korsakoff psychosis. For this reason, the two entities are often described together as WKS.

Alcohol abuse, AIDS, malignancy, hyperemesis gravidarum, prolonged total parenteral nutrition, iatrogenic glucose loading in any predisposed patient, and other disorders associated with grossly impaired nutritional status are associated with WKS.

Bariatric surgery (there are more than 100,000 weight-loss procedures performed annually in the United States) has been associated with both malnutrition and WE. Post–bariatric surgery patients have a limited capacity for food intake during the initial weeks after a bariatric procedure and a body's reserves of thiamine can be depleted after only 20 days of inadequate supply. Post–bariatric surgery patients may still be frankly obese when presenting with WE symptoms caused by thiamine deficiency.
Presentation
History
The three components of the classic triad of WE are encephalopathy, ataxic gait, and some variant of oculomotor dysfunction. However, a complicating factor of WE identification is that its presentation may not be associated with the classical clinical triad in up to 90% of patients.

Consideration for WE should be given to patients with any evidence of long-term alcohol abuse or malnutrition and any of the following: acute confusion, ataxia, ophthalmoplegia, memory disturbance, hypothermia with hypotension, and delirium tremens.

A high proportion of patients with acute WE who survive develop WKS, characterized by potentially irreversible retrograde amnesia (inability to recall information) and anterograde amnesia (inability to assimilate new information), with varying degrees of other cognitive deficits.[13]

Consider WE when any patient with long-term malnutrition presents with confusion or altered metal status. Significant overlap exists between WE and Korsakoff psychosis. For this reason, the two entities are often described together as WKS.

Alcohol abuse, AIDS, malignancy, hyperemesis gravidarum, prolonged total parenteral nutrition, iatrogenic glucose loading in any predisposed patient, and other disorders associated with grossly impaired nutritional status are associated with WKS.

Bariatric surgery (there are more than 100,000 weight-loss procedures performed annually in the United States) has been associated with both malnutrition and WE.[9] Post–bariatric surgery patients have a limited capacity for food intake during the initial weeks after a bariatric procedure and a body's reserves of thiamine can be depleted after only 20 days of inadequate supply. Post–bariatric surgery patients may still be frankly obese when presenting with WE symptoms caused by thiamine deficiency.[9]

Physical Examination
Ocular abnormalities are the hallmarks of WE. The oculomotor manifestations are: nystagmus, bilateral lateral rectus palsies, and conjugate gaze palsies reflecting cranial nerve involvement of the oculomotor, abducens, and vestibular nuclei. Less frequently noted manifestations are: pupillary abnormalities such as sluggishly reactive pupils, ptosis, scotomata, and anisocoria. The most common ocular abnormality is nystagmus, not abducens (Cranial Nerve VI) ophthalmoplegia.

Encephalopathy is characterized by a global confusional state, disinterest, inattentiveness, or agitation. The most common presenting symptoms of WE are mental status changes. Stupor and coma are rare.

Gait ataxia is often a presenting physical examination manifestation.[8] Ataxia is likely to be a combination of polyneuropathy, cerebellar damage, and vestibular paresis. Vestibular function, usually without hearing loss, is universally impaired in the acute manifestation of WE. In less severe cases, patients walk slowly with a broad-based gait. However, gait and stance may be so impaired as to make walking impossible. Cerebellar testing in bed with finger-to-nose and heel-to-shin tests may not illicit any notable deficit; thus, it is important to test for truncal ataxia with the patient sitting or standing.

In addition to ophthalmoplegia and ataxia, 80% of adults will have some degree of peripheral neuropathy, which may include weakness, foot drop, and decreased proprioception.

Thiamine deficiency has recently been associated with a gastrointestinal syndrome of nausea, vomiting, abdominal pain, and lactic acidosis.

Other symptoms that may occur in addition to, or in place of, the classic triad include hypothermia, hypotension, and coma. Thiamine deficiency often affects the temperature-regulating center in the brainstem, which can result in hypothermia.

Hypotension can be secondary to thiamine deficiency either through cardiovascular beriberi or thiamine deficiency–induced autonomic dysfunction. Coma is rarely the sole manifestation of WE.

Of patients surviving WE, an important percentage will manifest WKS, characterized by the following: retrograde amnesia (inability to recall information), anterograde amnesia (inability to assimilate new information), decreased spontaneity and initiative, and confabulation.

Other manifestations of thiamine deficiency involve the cardiovascular system (wet beriberi) and peripheral nervous system (nutritional polyneuropathy).

Manifestations of thiamine deficiency in infants are constipation, agitation, apathy, vomiting, lack of appetite, and later, diarrhea, grunting, nystagmus, convulsions, unconsciousness, and cardiomyopathy.

Mc Afee Regime

Mc Afee Regime
Conservative management of placenta praevia
(MCafee's regime)

- it's usually done if the fetus is preterm, patient usually has to be warded at 32 week until 38 weeks/delivery.
- if bleeding is not severe/spotting, advice for bedrest along with strict pad chart monitoring.
- monitor vital sign.
- ultrasound monitoring for placenta localization is done every 2 weeks to look for placenta migration, possible prior to 34 weeks since the lower segment formation is in the process of completion.
- fetal monitoring by ctg and biophysical profiling to ensure fetal well being.
- ask the mother to keep daily fetal kick chart.
- 2 doses of dexamethasone, 12mg administered IM 12 hours apart to enhance lung maturity and prevent interventricular hemorrhage in preterm babies.

-availability of 2 unit gsh
availability of c-sec

Placenta previa

Athirah Fikri: Salam dr
What is the use of MRI in investigation of placenta previa patient?

Umair: Mri is the gold standard imaging for pp as saggital images best demostrate the relationship of placenta to cervical os.

Ni yg saya baca sendiri dr. Is it correct? Sbb takde sekali dgn group yg dr mention hari tu.

 Umair: But in most situation it is not required since it can be detected by ultrasound

Dr Shaiful Ehsan: Dear my BELOVED juniors...
Remember events at 34 weeks?
I did mentioned about completion of lower segment?

Placental mapping should be done for those patient with histroy of I PREVIOUS scar plus current PP or anterior placenta on top of prev scar....

Modalities of placental mapping includes ultrasound...

MRI is indicated if ultrasound is inconclusive for accreta percreta but suspicions is high......

Placental mapping is done around 32 - 34 weeks...


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Antenatal care for asymptomatic complete PP.

https://www.google.com/url?q=http://article.sciencepublishinggroup.com/pdf/10.11648.j.cmr.20130201.11.pdf&sa=U&ved=0CDAQFjAEahUKEwjoxYuIpf3IAhUUSY4KHZB0BRQ&sig2=8xeXYVDfxV7ZKsb-9GBRQA&usg=AFQjCNF7mbx82OgO09IeS3d67e1pE9nLZQ