Kerley's Line (Septal Line)

Kerley’s A line
An essentially straight linear opacity 2–6 cm long and 1–3 mm wide, usually situated in an upper lung zone, that points to the hilum centrally and is directed toward but does not extend to the pleural surface.
These are longer (at least 2cm) unbranching lines coursing diagonally from the periphery toward the hila in the inner half of the lungs. They are caused by distension of anastomotic channels between peripheral and central lymphatics of the lungs. Kerley A lines are less commonly seen than Kerley B lines. Kerley A lines are never seen without Kerley B or C lines also present.

Kerley’s B line
An essentially straight linear opacity 1.5–2 cm long and 1–2 mm wide, usually situated in the lung base and oriented at right angles to the pleural surface with which it is usually in contact peripherally.
These are short parallel lines at the lung periphery. These lines represent interlobular septa, which are usually less than 1 cm in length and parallel to one another at right angles to the pleura. They are located peripherally in contact with the pleura, but are generally absent along fissural surfaces. They may be seen in any zone but are most frequently observed at the lung bases at the costophrenic angles on the PA radiograph, and in the substernal region on lateral radiographs. Kerley B lines are seen in Congestive Heart Failure (CHF) and Interstitial Lung Diseases (ILD).

Kerley’s C line
A group of branching, linear opacities producing the appearance of a fine net, situated at the lung base and representing Kerley’s B lines seen en face.
These are the least commonly seen of the Kerley lines. They are short, fine lines throughout the lungs, with a reticular appearance. They may represent thickening of anastomotic lymphatics or superimposition of many Kerley B lines.

A115262

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Chest X-Ray in Left Ventricular Failure

MNEMONIC
A - Alveolar Edema (Bat's Wing)
B - Kerley B lines (Interstitial Edema)
C - Cardiomegaly
D - Dilated prominent upper lobe vessels
E - Pleural Effusion





Thanks to Dr Shahul for asking this question during ward round.

A115262

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Some brainstem lesions & its manifestation

Lateral Medullary Syndrome is covered already.

Medial Medullary Syndrome/ Dejerine Syndrome

Causes :
Stroke of
-Anterior spinal artery
-Basilar Artery
-Vertebral Artery

Clinical features:
-Contralateral
Pyramidal Tract -> hemiparesis
Medial lemniscus (dorsal column) -> LO concious propioception, LO discriminative touch, LO vibration

-Ipsilateral
Hypogossal nerve -> deviation of tongue to the AFFECTED SIDE (weakness side)

Need help with this, very confusing. If the tongue deviates to the right, meaning the stroke is on right medial medullary ?

Extra : Locked-In Syndrome

Causes :
Stroke in Basilar Artery

Presentations:
-quadriplegia
-cannot speak (vocal cord is not paralysed, but voice and breathing is not coordinated well, hence reduced ability to speak)
-Retain full consciousness & cognitive function
-Eye movement & blinking is still retained -> can be used to communicate

Some call this as "pseudocoma"

by alvis

Thanks to Dr. Ngiu for asking us Wallenburg and thanks to Fadhli for posting that info and stimulate me to find the other brainsteam lesion

Source :
- Netter Neuroanatomy
- Oxford
- Year 2 lecture note
- http://www.strokecenter.org/prof/syndromes/index.htm
(If you guys are intesrested on stroke syndromes, can visit this site)

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Some random things about Chronic Liver Disease

Q1 : What to look for in chronic liver disease during PE ?

Signs of hepatic failure
- Jaundice ( skin + sclera + mucous membrane, conjugated + unconjugated bilirubin ) + scratch marks
- Hepatomegaly ( due to extramedullary haemopoiesis)
- Anaemia
- Purpura (coagulopathy - factor II, VII, IX & X)
- hypoalbuminaemia -> Ankle edema, +\- ascites, nail changes (Leukonychia, Muehrcke's Line), oedema
- Finger clubbing

Signs of hyperestrinism (Hyper-estrogen-ism) - because liver cannot breakdown estrogen and cannot synthesize estrogen binding protein
- Spider Naevi
- Pectoral alopecia
- Female : Breast atrophy (dun ask me, tak tahu kenapa. xD)
- Male : Gynecomastia, Altered Pubic hair distribution, testicular atrophy
- Loss of axillary hair
- Palmar Erythema

Signs of decompensated liver disease (Portal Hypertension)
- Hypersplenism -> splenomegaly, Pancytopenia -> Pallor conjunctiva
- Caput medusae (blood flow towards the legs, must differentiate from visible veins due to IVC/SVC obstruction)
- Ascites
- Venous Hum
- Esophageal varices -> Pallor conjunctiva

Causes of Chronic Liver disease
- Hepatitis -> tattoo, IVDU needle injection scar, tender liver
- Alcoholism -> Dupuytren's contracture, parotid swelling
- Haemochromatosis -> Hyperpigmentation of the skin
- Thalassemia -> Desferrioxamine infusion pump, thalassemia facies, laparotomy scar, slate-gray hyperpigmentation of skin, stunted growth (Chronic liver failure is a sign of iron overload in Thalassemia)
- Wilson's disease -> Kayser-Fleischer Ring
- Hepatocellular Carcinoma -> Liver bruit/rub, firm and irregular liver on palpation

Complications of chronic liver disease
- Hepatic encephalopathy -> drowsiness, confusion, asterixis, constructional apraxia (Ask patient to draw a 5 point star, see picture)
- Spontaneous Bacterial Peritonitis -> reduced bowel sound

Q2 : Why anemia happens in Chronic Liver disease ?
- Hypersplenism
- Anemia of chronic liver disease
- Poor nutrition due to chronic illness
- Oesophageal Varices

Q3 : Why Spironolactone is the diuretic of choice in decompensated chronic liver disease with portal hypertension & ascites ?
- Because spironolactone has aldosterone antagonist activity
- In chronic liver disease, liver cannot metabolize aldosterone -> Hyperaldosteronism
- Might further precipitate oedema & ascite -> very bahaya

Q4 : Which electrolytes imbalance can cause confusion ?
- ONLY Sodium, Urea & calcium !!!

Q5 : How to quantify alcohol intake per week ?
- Male should consume less than 21 unit
- Female less than 14 unit
- 1 can of beer = 1 unit
- 1 shot of whiskey = 1 unit
- 1 serving of wine (half glass) = 1 unit

Q6 : List out clinical signs of alcoholism
- Peripheral neuropathy
- Proximal myopathy
- Beri-beri heart (CCF) - due to thiamine deficiency
- Cerebellar signs (ataxia)
- Wernicke's encephalopathy -> CNVI palsy (lateral rectus)
- Korsarkoff's psychosis -> Amnesia, confabulation

Q7 : Patient has G6PD, how can you see from investigations/signs that patient is having haemolysis of RBC right now ?
- Serum haptoglobulin decrease
- LDH high
- Reticulocyte high
- Normocytic initially, might be macrocytic later (MCV high)
- Dark Urine

Sources :
-Ward rounds and teaching with Dr. Paras. Thank you Dr Paras, we love you and we will miss you. >.<
- Prof Izham's Short case & you
- Oxford Handbook
- Burton Aids
- Netter's clinical anatomy

by Alvis
Please correct me if I am wrong, or if there are any uncertainties, thanks.

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Wallenberg's Lateral Medullary Syndrome

CAUSE
Posterior Inferior Cerebellar Artery (PICA) occlusion
(lead to brainstem infarction)


FEATURES
dysphagia, dysarthria (IX and X nuclei)
vertigo, nausea, vomiting, nystagmus (vestibular nucleus)
ipsilateral ataxia (inferior cerebellar peduncle)
ipsilateral Horner's syndrome (descending symphathetic fibers)
loss of pain & temperature sensation on ipsilateral face (V nucleus)
loss of pain & temperature sensation on contralateral limbs (spinothalamic tract)
NO limb weakness (pyramidal tracts are unaffected)

Thanks to Dr Ngiu for showing us patient with Wallenberg's Lateral Medullary Syndrome.

A115262

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Pleural Rub

An elderly chinese gentlemen with a background hx of parkinson disease come to the A&E with dyspnea, fever and reduce counciousness since 2 days ago.

On examination he was dyspnoeic with RR of 28 + use of accessory muscle + course crepts + bronchial breath sound + pleural rub over the left upper zone.

What is your differential for pleural rub? - one MO ask...

• pleurisy - secondary to pneumonia or pulmonary infarction
• rare - pleural malignancy, spontaneous pneumothorax, pnemodynia

Describe the pt's tone (UL exam)

• cogwheel / plastic / leadpipe rigidity - ↑ tone with interrupted nature → muscle give way → jerks
• due to exagerated stretch reflex interrupted by tremor

Assess the pt's GCS score

• eye - 4
• motor - 1
• verbal - 1
• = 6

A114141

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C-peptide?

A 42-year-old woman is brought to the emergency room by ambulance for altered mental status. The glucose level by fingerstick monitoring was below the measurement capabilities of the monitor (<40 mg/dL). After 2 ampules of 50% dextrose, the patient’s fingerstick glucose remains at 42 mg/dL. She remains unconscious and had a 1-min seizure while in transport. She has no history of diabetes mellitus. Her family denies that she has been recently ill, but recently she has been depressed. She works as a registered nurse on a medical floor of the hospital.

Which of the following tests would confirm an overdose of exogenous insulin?
A. Plasma glucose <55>18 pmol/L, and plasma C-peptide levels undetectable
B. Plasma glucose <55>18 pmol/L, and plasma C-peptide levels >0.6 ng/mL
C. Plasma glucose <55 mg/dL, plasma insulin <18 pmol/L, and plasma glucagon <12 pmol/L
D. Plasma glucose <55 mg/dL, plasma insulin <18 pmol/L, and C-peptide levels undetectable

The answer is A.
When an individual presents with profound hypoglycemia and no history of diabetes mellitus, one must determine the cause expediently and treat accordingly. Immediate treatment of this patient should include ongoing glucose administration while attempting to determine the cause. The initial step for diagnosing this patient is to determine the plasma glucose, insulin, and C-peptide levels. When the plasma glucose level is <55 mg/dL, the plasma insulin levels should be low. If the insulin levels are inappropriately high (≥18 pmol/L or ≥3 μU/mL), the C-peptide level should be assessed simultaneously. C-peptide is the protein fragment that remains after proinsulin is cleaved to insulin. C-peptide would be high (≥0.6 ng/mL) in individuals with an endogenous source of hyperinsulinemia such as insulinoma. However, C-peptide levels are low or undetectable when the source of insulin is exogenous, such as in surreptitious insulin intake or insulin overdose. One exception to consider in this individual is surreptitious intake or overdose of a sulfonylurea, an insulin secretagogue. In this case, insulin and C-peptide levels would both be elevated, and a sulfonylurea screen is also appropriate in this patient.

A114141

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GN + hemoptysis = ?

A 54-year-old female presents to the hospital because of hemoptysis. She has coughed up approximately 1 teaspoon of blood for the last 4 days. She has a history of cigarette smoking. A chest radiogram shows diffuse bilateral infiltrates predominantly in the lower lobes. The hematocrit is 30%, and the serum creatinine is 4.0 mg/dL. Both were normal previously. Urinalysis shows 2+ protein and red blood cell casts.

The presence of autoantibodies directed against which of the following is most likely to yield a definitive diagnosis?
A. Glomerular basement membrane
B. Glutamic acid decarboxylase
C. Phospholipids
D. Smooth muscle
E. U1 ribonucleoprotein (RNP)

The answer is A.
A variety of autoimmune diseases may cause pulmonary/renal disease, including Wegener’s granulomatosis, microscopic polyangiitis, SLE, and cryoglobulinemia. Goodpasture’s syndrome is characterized by the presence of anti–glomerular basement antibodies that cause glomerulonephritis with concurrent diffuse alveolar hemorrhage. The disease typically presents in patients over 40 years old with a history of cigarette smoking. These patients usually do not have fevers or joint symptoms. Among the listed options, antibodies to glutamic acid decarboxylase are seen in patients with type 1 diabetes or stiff-man syndrome, anti–smooth muscle antibodies in patients with autoimmune hepatitis, and anti–U1 RNP in those with mixed connective tissue disease. Antiphospholipid antibody syndrome may cause renal disease and alveolar hemorrhage, but this usually occurs in the context of a systemic illness with prominent thrombosis in other organ systems [extremities, central nervous system (CNS)].

A114141

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Horner's Syndrome

oculosympathetic pathway involved in Horner's syndrome:

1. fibers from the hypothalamus go to the ciliospinal centre in the spinal cord at C8, T1 and T2.
2. synapse.
3. second-order neurones exit via the anterior ramus in the thoracic trunk.
4. synapse in the superior cervical ganglion in the neck.
5. third-order neurones travel from here with the internal carotid artery to the eye ( the pupil, the levator palpebrae) and the sweat glands of the face.

A lesion at any site along the pathway can produce Horner's syndrome.

Causes of Horner's syndrome:

1. carcinoma of the apex of the lung ( usually squamous cell carcinoma)

2. neck

- malignancy eg. thyroid

- trauma or surgery

3. lower trunk brachial plexus lesions

- Trauma

- Tumor

4. carotid arterial lesion

- carotid aneurysm or dissection

- pericarotid tumors (Raeder's syndrome)

- cluster headache

5. brainstem lesions

- vascular disease (especially the later medullary syndrome)

- tumor

- syringobulbia

6. syringomyelia (rare)

source: Talley

Thanks to Dr Ngiu for asking this question after bringing us to the patient with lateral medullary syndrome.

A111218

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Hering's Law

Abnormalities of the abducting eye in internuclear ophthalmoplegia reflect an adaptive process that helps overcome the adduction weakness of the opposite eye.

This response operates under the constraints of Hering's law of equal innervation: any attempt to increase the innervation to a weak muscle in one eye must be accompanied by a commensurate increase in innervation to the yoke muscle in the other eye.

Source : http://www3.interscience.wiley.com/journal/109677683/abstract

Thanks to Dr Ngiu for asking this question after showing us patient with Right Internuclear Ophthalmoplegia today.

A115262

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Internuclear Ophthalmoplegia

When a person looks to the side opposite the affected (right) eye, the following happens:

• The affected (right) eye, which should turn inward, cannot move past the midline. That is, the affected eye looks straight ahead.
• As the other eye (left) turns outward, it often makes involuntary, repetitive fluttering movements called nystagmus That is, the eye rapidly moves in one direction, then slowly drifts in the other direction.
• May have double vision.

Internuclear ophthalmoplegia (INO) is a manifestation of intrinsic brainstem disease.

It is caused by a lesion involving the medial longitudinal fasciculus between the abducens and oculomotor nuclei.

Typically INO results from conditions which produce ischemia or demyelination in the brainstem.

The chief clinical features are an adduction deficit in the eye on the side of the lesion and nystagmus in the contralateral eye on attempted lateral gaze.

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

Internuclear ophthalmoplegia is impairment of horizontal eye movements caused by damage to certain connections between nerve centers in the brain stem.

In internuclear ophthalmoplegia, the nerve fibers that coordinate both eyes in horizontal movements—looking from side to side—are damaged. These fibers connect collections of nerve cells (centers or nuclei) that the 3rd cranial nerve (oculomotor nerve) and the 6th cranial nerve (abducens nerve) originate from.

In older people, the disorder usually results from a stroke, and only one eye is affected.

In younger people, it usually results from multiple sclerosis, and both eyes are often affected.

Less common causes include Lyme disease, tumors, and toxicity due to a drug (such as tricyclic antidepressants).

Horizontal eye movements are impaired, but vertical ones are not.

The affected eye cannot turn inward, but it can turn outward.

http://www.merck.com/mmhe/sec06/ch096/ch096b.html

Thanks to Dr Ngiu for showing us the patient with RIGHT INTERNUCLEAR OPHTHALMOPLEGIA today. We really appreciate the findings as mentioned above.

A115262

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Common Short Cases in Professional Exams

RESPIRATORY
Pleural effusion
Pulmonary fibrosis in RA
Consolidation
Bronchectasis
COPD(when desperate)
Pneumothorax (never,bcoz is acute!)

CARDIOVASCULAR
Heart failure
Murmurs
Prostetic click
Ebstein anomaly w TR(beware of this pt,we may see him in Pro exam)

NEUROLOGY
Bulbar Palsy
Parkinsonism
Stroke
CN III
CN VII
Spinocerebellar ataxia(this pt come to our Pro exam every yr!!)

GASTROINTESTINAL
Ballotable kidney
hepatoslenomegaly

ENDOCRINE
Cushing's
Graves/TMN goiter
acromegaly

MISCELLENOUS
Psoriatic athropathy
SLE
Scleroderma
RA

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how old M.I?

How old M.I ??

Cardiac enzymes
FABP	+	+	+	-	-
Myoglobulin	-	+	+	-	-
CKMB	-	-	+	+	-
Troponin T/I	-	-	+	+	+
	30min-3h	3h-6h	6h-24h	24h-48h	48h-14days

thanks to : dato' jeya, hkl

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Cushing Reflex & Cushing Triad

Question during oncall at A&E PPUKM :
In head trauma patient, why there is bradycardia + increase blood pressure?

CUSHING REFLEX

The Cushing reflex is a hypothalamic response to ischemia, usually due to poor perfusion (delivery of blood) in the brain.

The Cushing reflex consists of an increase in sympathetic outflow to the heart as an attempt to increase arterial blood pressure and total peripheral resistance, accompanied by bradycardia.

The ischemia activates the sympathetic nervous system, causing an increase in the heart's output by increasing heart rate and contractility along with peripheral constriction of the blood vessels. This accounts for the rise in blood pressure, ensuring blood delivery to the brain. The increased blood pressure also stimulates the baroreceptors (pressure sensitive receptors) in the carotids, leading to an activation of the parasympathetic nervous system, which slows down the heart rate, causing the bradycardia.

The Cushing reflex is usually seen in the terminal stages of acute head injury.

The Cushing reflex was first described by Harvey Cushing in 1902.

source : http://signsandsyndromes.com/cushing-reflex

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CUSHING TRIAD

Cushing's triad is a sign of increased intracranial pressure.

It is the triad of :

1. Hypertension (progressively increasing systolic blood pressure)

2. Bradycardia

3. Widening pulse pressure (an increase in the difference between systolic and diastolic pressure over time)

Cushing's triad suggests a cerebral hemorrhage in the setting of trauma or an space occupying lesion (e.g. brain tumor) that is growing and a possible impending fatal herniation of the brain.

Cushing's triad is named after an American neurosurgeon Harvey Williams Cushing (1869-1939).

source : http://classictriads.com/triads/cushings-triad

Thanks to Dr Johar (A&E) for asking us these questions

Learning issue : Differentiate between Cushing's disease and cushing's syndrome?

A115262

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Aortic Regurgitation

causes of chronic aortic regurgitation:

1. rheumatic heart disease
2. congenital (eg. bicuspid valve; VSD - an associated prolapse of the aortic cusp is not uncommon)
3. seronegative arthopathy (esp. ankylosing spondylitis)
4. aortic root dilatation

• marfan's syndrome
• aortitis (sero -ve arthropathies, RA, tertiary syphilis)

causes of acute aortic regurgitation

1. infective endocarditis
2. marfan's syndrome
3. dissecting aneurysm of the aortic root

Severity of AR

positive LR indicate that the presence of a sign is likely to occur that much more often in an individual with the disease than in one without it. the higher the positive LR, the more useful is a positive sign.

negative LR increases the likelihood that the disease is absent if the sign is not present.

source: Talley

A111218

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Doctor asks : "This patient present with chronic cough. Investigations ?"

NO.1 RULE : Talk about everything you know. Don't be scared to impress your examiner, but only say things that you sure you know how to answer.

No.2 RULE : Try to answer in a way that you can "drag" the examiner into your world. Lead them to ask the questions that you know how to answer ! Impress them !

Source : Dr. Siva & Dr. Paras

Situation :

- Chinese Male
- Middle age
- Presents with chronic cough for 2 months
- Initially cough with sputum, which is whitish in colour
- For recent 2 weeks, associated with blood streaks
- a/w SOB & fever these 2 weeks
- Went to GP before for treatment

Random Fact 1 : Pleuritic chest pain includes CHEST PAIN ONLY DURING COUGHING. Thus, pleuritic chest pain means chest pain during inspiration or coughing. (Source : Dr Siva from A&E)

Question : Tell me how would you investigate this patient ?

Answer :

I would like to divide my approach to investigation in 2 ways, which are blood biochemical investigation, radiological investigations, and lastly, special tests.

Blood :

1. FBC

• Hb - Chronic cough -> Poor oral intake -> malnutrition -> anemic
• Hb - Sputum with blood streaks
• Hb - Anemia in mycoplasma pneumonia (atypical)
  
• White Cell count - Infections ?
• Neutrophils high - Bacteria
• Lymphocyte high - Virus
• Eosinophil high - allergy, parasire
• Monocyte high - Chemotherapy (Dr say will give distinction for anyway who answer this correctly xD)
• Lymphocyte low - suspect Legionella atypical Pneumonia
  

2. RP
- Signs of dehydration (Hypo Na, Hyper K)
- Hyponatraemia -> Legionella
- Signs of renal failure (Urea and cretinine high) - can happen in aypical pneumonia (Legionella)

3. LFT
- albumin - chronic illness -> albumin low
- ALT & AST - atypical pneumonia (Legionella) -> liver enzymes high

ABG
- assess oxygenation status

4.ESR
- Sensitive but not specific indicator for presence of disease
- Raised ESR -> any inflammation, age, anaemia (esp sickle cell anemia), polycythaemia
-> Therefore, when ESR is raised in sickle cell anemia, polycythaemia -> beware
- Very high ESR (>100mm/h) -> 90% predictive value for disease
- Used as indicator for chronic disease

5.CRP
- Same with ESR, but changes more rapidly
- Increase in hours, and falls within 2-3 days
- Usage : Monitor response of therapy and disease activity

6. Blood C&S
- Both aerobic & anaerobic
- Atypical serology

7. Sputum AFB, C&S 3 times, early morning sample (Why early morning ? I x tau. Please post here if you know why, thanks ! ^.^)

8. Blood Culture

8. Mycobacterium PCR

9. Urine UFEME, C&S (x tahu kenapa, lupa dah, masa tu oncall, letih xD)

10. Serum Tumour Marker
- Not routinely done, but result might be positive -> (Chronic disease give elevated tumour marker)
- Lung Ca doesn't have any tumour marker

Radiological :

1. CXR
- Signs of pneumonia ?
- Signs of malignancy ? - well defined circumscribed lesion, cannonball appearance,
if have, go for CT thorax
- TRO Pneumothorax, pleural effusion

2. ECG
- TRO CVS causes

Special tests:

1. LN Biopsy
- If any palpalble LN

2. Mantoux Test

3. Pleural Tap if any evidence of pleural effusion

Source : Dr. Siva & oxford

Random Fact 2 :
Elderly patient was hospitalized before for a long time due to infection. Discharged well. Came back with diarrhoea after 1 week, why ?

Answer : Pseudomembranous Colitis

Because of old age, and prolong antibiotic (esp if IV), normal flora of the guts are killed. Then, obergrowth of Clostridum Difficile, cause pseudomembranous colitis.

Tx : Metronidazole, or, Oral Vancomycin

Patient can also come back with SOB -> Hospital acquired Pneumonia

Source : Dr Ilyaas

By alvis

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Tetralogy of Fallot

Tetralogy of Fallot is treated surgically. A temporary operation may be done at first if the baby is small or if there are other problems. Complete repair comes later. Sometimes the first operation is complete repair. Placement of a BLALOCK-TAUSSIG SHUNT (BTS) is a 'closed-heart' procedure performed as a first stage to correct TOF. Placement of a shunt is usually a temporary measure designed to alleviate symptoms until such time that the patients is in better condition to undergo complete repair.

BTS (An incision is made on the side of the chest under the arm, extending up towards the scapula).

The significant problem in TOF is REDUCED blood flow into the lungs. This results in reduced oxygen delivery to the body.

The operations designed to increase blood flow into the lungs are called SYSTEMIC-PULMONARY SHUNTS. These are connections between aorta or one of its branches (the "systemic" arteries / subclavian artery) and the pulmonary artery. The principle underlying these shunts is that a portion of blood flow from the arteries will ne directed across the shunt into the pulmonary artery and its branches. This has 2 effects :

• First, by increasing the total lung blood flow, the amount of oxygen available for distribution to the rest of the body is increased.
  
• Second, the increasing amount of blood flowing into the pulmonary artery and its branches stimulates them to grow in size. The narrow portions may become wider. So, later, when an operation for total correction is performed, there is little or no obstruction to lung blood flow.

Patient who have had completely repair of this condition in infancy may present with particular problems.

Repair of the right ventricular outflow obstruction and enlargement of the pulmonary valve annulus may leave severe pulmonary regurgitation which may lead eventually to exertional dyspnoea.

The surgery itself has, until recently, required a right ventriculotomy (cutting into the right ventricle). this leave a scar that can be associated with cardiac rhythm abnormalities in later life. patients may present with palpitations or syncope.

Signs may include:

• a median sternotomy scar,
• a long diastolic murmur of pulmonary regurgitation and signs of right ventricular enlargement (parasternal impulse)
• and later of tricuspid regurgitation (big v waves in the neck and a pulsatile liver).

Thanks to Dr Ngiu for asking us about BTS and how to know the patients had done the operation for TOF, any signs?

Sources :

Talley O'Connor Clinical Examination

http://www.chdinfo.com/aa/aa112397.htm,

http://www.debakeydepartmentofsurgery.org/home/content.cfm?proc_name=Blalock-Taussig+Shunt+Placement&content_id=272

A111218

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Assessment of Severity of Valvular Defects

click on the image to enlarge it

Thanks to Dr Ngiu for asking us the question on assessment of severity of aortic regurgitation.

Source : X'press Revision in Short Cases, Aids to Undergraduate Medicine

Learning issue : List down the peripheral signs of aortic regurgitation.

A115262

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Metered-Dose Inhaler

INSTRUCTION FOR USE

Take one dose at a time.
Remove the cap and shake the inhaler several times.
Sit upright, hold head up and breathe out.
Place inhaler in mouth and seal lips around mouthpiece.
Breath in, press the canister down (The canister should be pressed just after the start of inhalation, not before) to release the drug and continue to take a deep breath in.
Remove inhaler and hold breath for as long as possible up to 10 seconds.
Then expire through nostril slowly.
Recover (how long?) before taking the next dose, replace cap.

*this MDI + spacer


Sources of information : Oxford Handbook of Clinical Examination and Practical Skill

A115262

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BP Measurement (mercury column sphygmomanometer)

CHECK THE BP SET

The key to the reservoir should be turned open
The mercury meniscus should be at zero
The calibrated glass tube must be clean – a dirty tube can cause inaccurate readings.

CUFF SIZE

The bladder length should encircle at least 80% of the circumference.
The width should be at least 40% of the circumference of the arm.
Too small a cuff will give a falsely higher reading and vice versa.


INFLATION-DEFLATION BULB

The following may indicate malfunction of the device:
# Failure to achieve a pressure of 40 mmHg above the estimated SBP or 200 mmHg after 3–5 seconds of rapid inflation.
# The inability of the equipment to deflate smoothly at a rate of 1 mmHg per second or at each pulse beat.

AUSCULTATORY MEASUREMENT

Patients should be adequately rested and seated with their arms supported.

The cuff and the mercury reservoir should be at the level of the heart.

They should not have smoked or ingested caffeine within 30 minutes of measurement.

The SBP should be estimated initially by palpation. While palpating the brachial/ radial artery, the cuff is inflated until the pulse disappears. The cuff should then be inflated to a further 20 mmHg. The cuff is then slowly deflated and the pressure at which the pulse is palpable is the estimated SBP.

The bladder is again inflated to 20 mmHg above the previously estimated SBP and the pressure reduced at 1-2 mmHg per second whilst auscultating with the bell of the stethoscope.
The bell should not be placed under the cuff.

The point at which repetitive, clear tapping sounds first appears (Korotkoff Phase I) gives the SBP.

Phase I sounds sometimes disappear as pressure is reduced and reappears again at a lower reading (the auscultatory gap), resulting in underestimation of the SBP.

The complete disappearance of sound (Korotkoff Phase V) should be taken as the diastolic reading.

In some groups, e.g. anaemic or elderly patients, the sounds may continue until the zero point. In such instances the muffling of the repetitive sounds (Korotkoff Phase IV) is taken as the diastolic pressure. The point of muffling is usually higher than the true arterial diastolic pressure. If Korotkoff Phase IV is used, this should be clearly recorded.

BP should be measured in both arms and the higher reading is taken as the systemic BP.
If the difference in BP between the two arms is >20/10 mmHg, there may be an arterial anomaly which requires further evaluation.

POSTURAL DROP

The BP should be taken both lying and at least one minute after standing to detect any postural drop, especially in the elderly and in diabetics. On rising, the BP will transiently rise and then fall. A systolic drop of >20 mmHg is considered a significant postural drop.

source : Ministry Of Health Malaysia

learning issue : what is Korotkoff Phase?

A115262

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Barrel Chest

EVIDENCE OF BARREL CHEST

Increase antero-posterior diameter
Loss of cardiac and liver dullness
Reduce space between costal margin and ASIS (usually can place 2 hands)
Liver ptosis
At rest, ribs are not in oblique but persistently in horizontal position
Reduce space between trachea and suprasternal notch (normally can insert 2 fingers)


Thanks to Prof Shahrir
Thanks to commentator below for correcting the facts.

Learning issue : What are the differential diagnoses for barrel chest?

A115262

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Differential Clubbing

Differential Clubbing
Clubbing limited to upper or lower limbs alone.
Clubbing may be limited to the upper limbs in chronic obstruction of veins of the upper thorax.
A common cause is phlebitis of the upper extremities as seen in IV drug users

Differential Clubbing In the Lower Limbs Only
It may be associated with cyanosis of the lower limbs.
It is classically due to PDA with reversal of shunt( Eisenmenger PDA).
It is also seen in in infected abdominal artery aneurysm.

Thanks to Dr Ngiu for asking us these question
Answer from this website.

Learning Issue 1 : what is the grading for clubbing?

Learning Issue 2 : what are the differential diagnosis for clubbing?

A115262

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Warning Sign in Dengue

CLINICAL
abdominal pain / tenderness
persistent vomiting
clinical fluid accumulation
mucosal bleeding
lethargy
restlessness
hepatomegaly >2cm

LABORATORY
increase haematocrit concurrent with rapid decrease in platelet count

source : HKL

learning issue : what does warning sign indicate?

A115262

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Chest Pain with Low BP and High HR

Chest Pain with Low BP and High HR

How to manage this patient?

1
Inotrope (e.g. Digoxin)
to stabilise blood pressure first

2 (a)
B-blocker (e.g. propranolol)
to reduce heart rate

2 (b)
(if B-blocker contraindicated e.g. in asthmatic)
Calcium channel blocker which act centrally (e.g. diltiazem, verapamil)
to reduce heart rate

Others
ACEi / ARB
Diuretic


Credits to Kanit and Asilah's group for teaching me.

* Learning issue : why the patient who take ACEi presented with cough as side effect?

A115262

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