Prezi Presentation

I learnt of this new presentation software called "Prezi", which can make presentations actually fun to create and watch at the same time.

I'm bored of powerpoints, so it's quite refreshing for me to be able to make some interactive-looking stuff easily with a click of a mouse.

Made an elective posting presentation using this software;

http://prezi.com/eslrmcauimux/presentation-of-jgroopmans-book-how-doctors-think/#share

its most useful for conceptual presentations, i think.

CME - Appendicitis - Dx and Presurgical Management.

Update on appendicitis: Diagnosis and presurgical management - Janet H Friday

• Diagnostic tests - overview (what is being done now?)
• Hx, PE, WBC, CRP levels
• MANTRELS score
• Movement of pain to RIF
• Anorexia
• Nausea
• Tenderness in RIF
• Rebound tenderness
• Elevated temperature
• Leukocytosis
• Shift of WBC to left
• Diagnostic imaging
• US,
• IV contrast CT
• Issues with the current diagnostic methods
• MANTREL score has low sensitivity (76-90%) and specificity (50-81%)
• Abdominal CT has the best individual test, but it may be being carried out too rapidly.
• Diagnosing Appendicitis with Ultrasound
• 14 published studies cited including over 10000 children who underwent US scans for evaluation of possible appendicitis
• Sensitivity varied from 50-100%
• Specificity ranges from 88-99%
• Which means negative US scan does not exclude appendicitis unless normal appendix correctly visualized.
• Imaging protocol
• Every patient undergo US before CT scan
• If US inconclusive / negative, CT performed
• This has resulted in 22% of patient CT avoidance.
• Some people may be better off doing US
• Adolescent female - blood supply to ovaries can be obvserved.
• Thin people - easier to visualize internal organs
• Children - CT contraindicated due to radiation
• Diagnosing Appendicitis with CT
• Dx with CT scan has sensitivity of 97%, specificity of 94%^[i]
• Contrast-enhanced CT seem to have a higher reliability than non contrast CT-enhanced CT.
• The issue with CT
• Since the publication of reports of diagnostic accuracy of CT, the CT scans in children has increased seven-folds in US^[ii]
• In one year, 753 patients assessed for appendicitis (2001), where 172 were <18. In this group, 138 (80%) went thru CT scanning for suspected appendicitis, and 62(45%) were negative.
• Unnecessarily CT scans are being performed.
• New clinical decision rule
• Kharbanda et al^[iii]
• Nausea (2 pts)
• Hx of focal right lower quadrant pain (2pts)
• Migration of pain (1pt)
• Difficulty walking (1pt)
• Rebound tenderness (2pts)
• Absolute Neutrophil Count more than 6.75x10­³ (6pts)
• Score up to 5 had a sensitivity (of no appendicitis) of 96%, a negative predictive value of 96%.
• A recursive-partitioning model was created, and the following variables were found to be important
• ANC > 6.75x10³
• Nausea (emesis and anorexia were surrogate variables)
• Maximal tenderness in RLQ.
• When all 3 were absent, the rule had sensitivity of 100% for identifying low-risk patients.
• Presurgical management - analgesics
• According to Kim et al^[iv] and Kokki and associates^[v]
• Analgesic use in children will not affect the diagnostic accuracy of appendicitis.
• Analgesia may be given before surgeon’s examination.
• Use of analgesia may be acceptable especially when waiting for the consultant to arrive.
• Presurgical management - Antibiotics
• 45 published studies of 9576 adults and children with appendicitis who were randomized to be given either antibiotics or placebo before, during, or after appendectomy
• Use of antibiotics were superior to placebo for preventing wound infection and intra-abdominal abscess, regardless of whether perforation has occurred.
• Recent recommendation
• Meropenem
• Imipenem
• Ampicillin, gentamycin, clindamycin (generic)

Take home message - MANTRELS scoring may be outdated - we need to look at ANC values, consider US before CT, can use analgesics, good to use antibiotics presurgically.

---

[i] Garcia Pena et al Ultrasonography and limited computed tomography in the diagnosis and management of appendicitis in children. JAMA 1999; 15:1041-1046

[ii] National Caner Institute. Radiation and Pediatric computed tomography: a guide for health care providers. Summer newsletter; 2002 1-4

[iii] Kharbanda AB, Taylor GA, et al A clinical decision rule to identify children at low risk for appendicitis. Pediatrics 2005; 116:709-716

[iv] Kim MK, Strait RT, Sato TT, et. Al. A randomized clinical trial of analgesia in children with acute abdominal pain. Acad Emerg Med 2002; 9:281-287

[v] Kokki H, Lintula H, Vanamo K, et al. Oxycodone vs placembo in children with undifferentiated abdominal pain; a randomized, double-blind clinical trial of the effect of analgesia on diagnostic accuracy. Arch Pediatr Adolesc Med 2005; 159:320-325

ECG

·         Many types of ECG

o    Holter monitor

§  The patient wears it for a long time - when patient experience discomfort, they may press a button to record it.

o    Ambulatory ECG

o    12-lead ECG

·         When you see an ECG…

o    Look at the rhythm

§  Usually, there is a R-R variation - sinus arrhythmia.

§  If not - may be diabetic neuropathy (no SA node reaction to vagal stimulation)

o    Look at the rate

§  Fast method - divide 300 by the number of big boxes.

§  Accurate method - divide 1500 by number of small boxes

o    P wave

§  Shows SA node activity

§  Inversion of P-wave (junctional rhythm)

·         Sometimes P wave inside QRS

·         Inversion of P wave plus slow conduction is usually indicative of junctional rhythm

·         In a junctional rhythm, the conduction does NOT start from atrium. From AV node instead

§  Sometimes P wave is absent - junctional bradycardia

·         In junctional bradycardia, usually rate = 40 to 60

§  If P wave is present but sometimes missing / irregular / dysmorphic, the beat may originate from the atrium BUT not from SA node.

·         It may be a wondering pacemaker if the P wave is “misbehaving”

§  Saw-tooth appearance

·         Several P waves per QRS - atrium firing impulse rapidly, but each beat not getting permitted to enter the ventricles.

o    Atrial flutter.

o    In atrial flutter, you would like to count the PP- rate and RR rate ratio. - see if the heart block is varying  / uniform.

o    In atrial flutter - the saw-tooth pattern is nice and regular - NEW saw - as compared to atrial fibrillation - where you would have an OLD saw.

·         Sometimes P wave occurs alone - without a QRS - if this happens uniformly, i.e. every 2 beats, or 3 beats, it is a heart block.

o    QRS complex

§  When QRS narrow (less than 3.5 small boxes), the impulse is proper in the ventricles - the arrhythmia is supraventricular

§  When QRS broad, the arrhythmia is ventricular arrhythmia (broad QRS complex tachycardia)

o    Tiny, vertical pulse just before a broad QRS complex - it may be a pacemaker artifact. (ventricular pacemaker artifact)

o    avR

§  is always negative in normal ECG - a positive AVR may suggest dextrocardia

o    ST segment

§  REGIONAL changes in ST segment suggests MI - if it is systemic, e.g. drugs, neurogenic, electrolyte etc the whole ECG changes.

§  Differential diagnosis of ST elevation

·         Intrinsic myocardial disease (e.g., myocarditis, ischemia, infarction, infiltrative or myopathic processes)

o    Contiguous leads elevations diagnostic

·          Drugs (e.g., digoxin, quinidine, tricyclics, and many others)

·          Electrolyte abnormalities of potassium, magnesium, calcium

·          Neurogenic factors (e.g., stroke, hemorrhage, trauma, tumor, etc.)

·          Metabolic factors (e.g., hypoglycemia, hyperventilation)

·          Atrial repolarization (e.g., at fast heart rates the atrial T wave may pull down the beginning of the ST segment)

·          Ventricular conduction abnormalities and rhythms originating in the ventricles

o    T wave

§  In the normal ECG (see below) the T wave is always upright in leads I, II, V3-6, and always inverted in lead aVR

§  The normal T wave is usually in the same direction as the QRS except in the right precordial leads e.g. V2

§  Also, the normal T wave is asymmetric with the first half moving more slowly than the second half.

§  Electrolyte changes

May be seen in the T-wave (tall, tenting T-wave in hyperkalemia etc )

Murmurs

In clinical schools (in Malaysia, at least) you will actually get to hear lots of murmurs, and you will see (if you take some time to look at them) lots of changes in the JVP

this is where we would need to actually comment on those murmurs and JVP findings, if we haven't already memorized everything about them (I know I haven't.)

murmurs


murmurs are reported according to their 4 main properties.

1. timing
2. site and radiation
3. loudness and pitch (grading if possible)
4. relationship to posture and respiration

the 4 characteristics will help us in determining just what kind of problem (usually valvular) are there, in the heart.

how do we know what is a systolic and diastolic murmur?

we palpate the carotid, for the pulsation. the heart sound that corresponds / occurs simulataneously with the pulsation is the S1, and any murmur that occurs between S1 and S2, is a systolic murmur.

now that we know what is systolic and what is diastolic, lets say the patient has a systolic murmur.

let us come up with a DD of a systolic murmur. 

• pansystolic
• VSD
• Tricuspid regurgitation
• mitral regurgitation
• ejection systolic
• pulmonary stenosis
• aortic stenosis
• HOCM
• fever / fit, young adults
• late systolic
• tricuspid regurgitation
• mitral regurge 
• prolapsed valve
• mitral Valve Prolapse

so how do we narrow this down? 

is is through the other maneuvers you could do, and also radiation.

systolic murmur

• pansystolic murmur (1st and 2nd heart sounds cannot be heard separately in all areas)
• is it left side (mitral regurge) or right (pulmonary regurge)? how to determine that?
• ask patient to breath in and out deeply
• a left-sided murmur (MR) will INCREASE in intensity with EXPIRATION as the venous return is reduced (as we breathe out, the intrathoracic pressure go down - making it easier for the left heart to pump blood)
• confirmed with M shaped P wave on ECG, and Echo.
• a right sided murmur (PR) will INCREASE in intensity with INSPIRATION as the venous return is increased (as we breathe in, intrathoracic pressure rises - pushing more blood into right heart)
• VSD will have no radiation - the murmur is heard throughout the precordium.
• confirmed by Echo and ECG - Right axis deviation & RBBB
  
• mid-systolic murmur (between S1 and S2, but both heart sounds heard clearly apart)
• Aortic stenosis
• cold extermities
• slow-rising pulse
• low BP
• low Pulse pressure
• HOCM
• JVP has high a wave, 
• thrillss and murmur at left sternal edge
• Aortic sclerosis
• more common in elderly with Atherosclerosis
• plumonary high flow
• typical in young women
• benign if no pulmonary hypertension
• ASD
• pulmonary stenosis
• low pulse
• increased JVP
• left parasternal heave

diastolic murmur

• mitral stenosis
• tapping apex
• rumbling in character
• mireal stenosis with pliable valve
• opening snap
• aortic regurgitation
• increased BP
• increased pulse pressure
• collapsing pulse
• displaced apex

TBL - Jaundice and Hepatitis

jaundice / hepatitis

jaundice

Jaundice is a yellowish colouration of the tissue resulting from the deposition of bilirubin

This only happens in the presence of serum hyperbilirubinemia, and is a sign of either

·         Liver disease

·         Hemolytic disorder (less commonly)

The degree of bilirubin elevation can be estimated by PE.

Sclera icterus = at least 51micromol/L (3mg/dL)

May be even green in colour if long-standing (oxidation of bilirubin to biliverdin)

Differential of yellow skin

·         Caretenoderma

·         Quinacrine

·         Phenol exposure

Increased bilirubin occurs when there is an imbalance between the production and clearance of bilirubin.

It may result from

·         Over-production of bilirubin

·         Impaired…

o    Uptake

o    Conjugation

o    Excretion

·         Regurgitation of unconjugated / conjugated bilirubin from damaged hepatocytes / bile ducts.

Initial steps in jaundice patient evaluation

History taking

Some presentation of jaundice are quite characteristic, and such history presentation should warrant a confirmatory  investigations.

·         Fever + nausea + Anorexia (even cigarettes also does not want)

o    Suggestive of viral hepatitis

§  Comfirmation by HepA IgM, Hep B surface antigen, Hep C IgM etc.

·         Pruritis + dark urine + pale stools

o    Suggestive of cholestasis

§  Check by bilirubin study (urobilinogen,

§  Alkaline phosphatase

§  Ultrasound of bile ducts

·         Fatty food triggers colicy pain

o    Suggestive of bile stone causes

§  Ultrasound

§  ERCP

·         Progressive jaundice + fever + chills + rigors (Charcot’s triad)

o    Stone obstructive cholangitis

§  ERCP

§  Ultrasound

·         Jaundice + fever + Conjuctivitis + muscle aches + passage of small and dark urine

o    Leptospirosis

§  Darkfield microscopy

·         Recurrant mild jaundice which worsen with fasting / fever

o    Gilbert syndrome

·         Hematemesis + easy brising, mental confusion, inverted sleep pattern after severe illness like CHF, Shock etc

o    Liver insufficiency causing hepatic encelopathy

§  Liver function tests

Physical examination

Physical examination is often useful, after a sufficient history has been taken from the patient.

History and physical exam should come hand in hand, to provide a solid Differential Diagnosis for us to proceed onto the investigations.

Investigations

·         Full blood count

o    To rule out hemolytic causes

o    Leucocyte – bac. infection

·         Liver biochemistry

o    To rule out hepatocellular causes

·         Bilirubin study

o    Conjugated hyper bilirubinemia

§  Hepatocellular origin

o    Unconjugated
hyper bilirubinemia

§  Over production,

§  Impared hepatic intake

§  Impared conjugation

·         Viral Markers

o    hepatitis viruses

o    EBV

o    CMV

·         Serum alpha-fetoprotein

o    Hepatocellular carcinoma,

o    Germ cell tumors

o    metastatic cancers of the liver.

·         Serum Albumin:

o    low level indicative of chronic liver disease.

·         Prothrombin Time:

o    sensitive indicator of chronic liver disease. Will be prolonged. Vitamin K deficiency must be excluded.

·         Aspartate Aminotransferase:

o    increased in hepatic necrosis, MI, muscle injury, CCF

·         Alkaline Phosphatase:

o    increased in cholestasis(intra/extrahepatic), metastasis of liver, cirrhosis.

·         Ȣ-Glutamyl Transpeptidase:

o    increases with alcohol consumption and drugs i.e. phenytoin

imaging

·         Ultrasound Imaging

o    Bile duct imaging

o    Gallstones?

o    Hepatic mets?

o    Pancreatic mass?

·         CT Scan

o    Abdominal malignancy?

o    Masses in abdomen?

·         Endoscopy (ERCP)

o    Bile duct opening

o    Bile duct obstruction

algorhythm of jaundiced patient (from Harrison 16th ed)

polyuria / polydipsia

Polyuria

When we talk of polyuria, we must first make sure we know what it means.

·         Polyuria is defined by a urine output of more than 3literes per day (hence 24 hour urine collection is essential)

·         It must be distinguished from frequency of urination which is just more frequent urination and not necessarily the amount of urine output.

Potential mechanisms of polyuria includes;

·         Excretion of nonabsorbable solutes (e.g. glucose) SOLUTE DIURESIS

·         Excretion of water (usually from a defect in ADH production or renal responsiveness) WATER DIURESIS

How do we know whether the patient is having a solute / water dieresis?

·         Urine osmolality measurements

o    Usual person excretes between 600-800 mosmol of solutes per day

§  As urea and electrolytes

o    Urine output is >3litres per day, and urine is dilute (<250mosmol / Litre), then total amount of solutes excreted is normal, and patient is having WATER DIURESIS.

§  Arising from

·         Polydipsia

·         Inadequate secretion of ADH (central DI)

·         Failure of renal tubules to respond to vasopressin (nephrogenic DI)

o    Urine output is >3 litres per day, and urine is >300mosmol/litre, then a SOLUTE DIURESIS is present, and the solute responsible for it must be found out, like;

§  Glucose

§  Mannitol

§  Urea

§  Diuretics

o    Poorly controlled diabetes with glucosuria is the most common cause of solute dieresis, leading to volume depletion and serum hypertonicity.

polydipsia

The primary stimulus for water ingestion is thirst, which is mediated by …

·         Increase in effective osmolality

·         Decrease in ECF volume or blood pressure

The osmoreceptors

·         Located in the anterolateral hypothalamus

·         Stimulated by a rise in tonicity

Urea and glucose does NOT play a role in stimulating thirst.

GALS Screening

GALS Screen

GALS stands for;

Gait
Arms
Legs
Spine

this is a systematic approach to a rheumatological system examination.

Order of examination - throughout the GALS screen

o    ask

o    Look

o    Feel

o    Move

Ask

o    Stiffness / pain  in any joints

o    Climb up / down stairs with ease?

o    Can you clothe yourself?

Gait

o    Walking rhythm

o    Pelvis and arm symmetry

o    Normal stride length

o    Ability to Turn quickly

Arms

o    Shoulder joint

§  Scars

§  Deformities

§  Normal muscle bulk

§  External rotation of shoulder

§  Full elbow extension

o    Hands

§  inspection

·         Swelling

·         Interosseous muscle wasting

o    Disuse atrophy

·         Swelling in PCP, MCP etc

·         Thenar and hypothenar wasting

o    Carpal tunnel $

·         Palmar erythyma

o    Occurs in 30% of RA patients

§  Palpation

·         Feel temperature

·         Squeeze the MCP joints

o    Any tenderness - inflammatory joint pathology

·         Press / feel individual joints

o    Cystic

§  Ganglion, abscess

o    Bony

§  Nodes (herbaden’s, bouchard’s)

o    Boggy

§  cynovitis

§  movement

·         Ask to make tight fist

·         OK sign

o    Nails

§  Psoriasis

§  Vasculitis

·         SLE

o    Elbows

§  Psoriatic patches

§  Rheumatic nodules

§  Straighten elbow

o    Compound

§  Hand to head

§  External rotation of shoulder

Legs

·         Feet

o    Metatarsal squeeze

o    Any eythyma

o    Swelling

o    Deformities

o    Callosities of sole

o    crepitus

·         Knees

o    Scars

o    Deformity

·         Knees

o    Feel for any bulge

o    Flexion of knees

o    Flex knees - and rotate externally - test pelvic joint

Spine

·         Kyphoscoliosis

·         Symmetrical muscle bulk

·         Level of iliac crest

·         Side

o    Curvature - scoliosis

o    Lumbar spine and hip flexion

·         Front 

• o     Lateral cervical flexion

o    Hyperalgesic response of fibromyalgia

·         Movement

o    Shober’s test

it is also good to know the RA criteria - 

The 2010 ACR-EULAR classification criteria for rheumatoid arthritis

	Score
Target population (Who should be tested?): Patients who have at least 1 joint with definite clinical synovitis (swelling)* with the synovitis not better explained by another disease†
Classification criteria for RA (score-based algorithm: add score of categories A–D; a score of ≥6/10 is needed for classification of a patient as having definite RA)‡
A. Joint involvement §
1 large joint¶	0
2-10 large joints	1
1-3 small joints (with or without involvement of large joints)#	2
4-10 small joints (with or without involvement of large joints)	3
>10 joints (at least 1 small joint)**	5
B. Serology (at least 1 test result is needed for classification)††
Negative RF and negative ACPA	0
Low-positive R/F or low-positive ACPA	2
High-positive RF or high-positive ACPA	3
C. Acute-phase reactants (at least 1 test result is needed for classification)‡‡
Normal CRP and normal ESR	0
Abnormal CRP or abnormal ESR	1
D. Duration of symptoms§§
<6 weeks	0
≥6 weeks	1