AF control

The initial management of patients with AF and a rapid ventricular rate involves two decisions:

• Determining the urgency of initial therapy (eg, intravenous versus oral rate control therapy, and/or immediate versus elective cardioversion).
• Choosing between a rate control and a rhythm control strategy.

Rate vs rhythm - AFFIRM and RACE trial has shown that rate and rhythm control have similar outcomes.

Rate control

Beta-blockers, usually metoprolol. IV for acute control, oral for chronic control

Complications: worsening heart failure, bronchospasms(COPD), hypotension, reduced exercise tolerance.

CCB, usually verapamil. Verapamil increases refractoriness and decreases conduction velocity in the AV node. These drugs can be used intravenously for acute rate control and can produce long-term rate slowing when used orally.

Digoxin, lows the ventricular rate during AF primarily by vagotonic inhibition of AV nodal conduction. It is generally less effective for rate control than beta blockers or calcium channel blockers, particularly during exercise when vagal tone is low and sympathetic tone is high (see 'Comparative efficacy' below [10,17,18,34-39]. Furthermore, digoxin has no ability to terminate AF. In HF, increases contractility and reduction in ventricular rate.

Plasma digoxin levels should be monitored periodically. Although the correlation between drug concentration and ventricular rate control is poor, the presence of a low serum digoxin concentration is useful in that it allows a higher dose to be administered.

Junctional escape beats (detected by the equality of all of the longest observed R-R intervals on the electrocardiogram) are common when digitalis has successfully slowed the ventricular rate. Giving more digoxin in this setting will increase the degree of AV nodal block and produce periods of a regular junctional escape rhythm. The change from single junctional escapes to periodic junctional rhythm usually signifies the development of digoxin toxicity.

Rhythm control

Reversion to NSR - pharmacological or direct cardioversion

DC cardioversion is indicated in patients who are hemodynamically unstable, a setting in which the AF is typically of short duration. In stable patients in whom spontaneous reversion due to correction of an underlying disease is not likely, either DC or pharmacologic cardioversion can be performed (table 2 and table 3A-B). Electrical cardioversion is usually preferred because of greater efficacy and a low risk of proarrhythmia. The overall success rate (at any level of energy) of electrical cardioversion for AF is 75 to 93 percent and is related inversely both to the duration of AF and to left atrial size [13]. (See "Restoration of sinus rhythm in atrial fibrillation: Therapeutic options".)A number of antiarrhythmic drugs are more effective than placebo, converting 30 to 60 percent of patients [14]. Evidence of efficacy from randomized trials is best established for ibutilide, flecainide, dofetilide, propafenone, and amiodarone

No structural heart disesae - fleclanide
Structural heart disease - amiodarone or sotalol

How to sedate a patient.

Summary:

• For severely violent patients requiring immediate sedation, give a rapidly acting typical antipsychotic or benzodiazepine alone (droperidol or midazolam) or a combination of a typical antipsychotic and a benzodiazepine (eg, haloperidol and lorazepam).
• For patients with agitation from drug intoxication or withdrawal, give a benzodiazepine.
• For patients with undifferentiated agitation, we prefer benzodiazepines, but typical antipsychotics are a reasonable choice.
• For agitated patients with a known psychiatric disorder, we prefer typical antipsychotic agents, but atypical antipsychotics are a reasonable choice.

Therefore,

• Haloperidol (5mg IM) + lorazepam (2mg IM) /diazepam[Pref. IV or oral (5-10mg)/midazalam[ I.V.: Initial: 0.5-2 mg slow I.V. over at least 2 minutes; slowly titrate to effect by repeating doses every 2-3 minutes if needed; usual total dose: 2.5-5 mg; use decreased doses in elderly.]
• or olanzapine (S/L wafer)
• Consider resperidone.
  
• Haloperidol has been used effectively for many years to control violent and agitated patients [69,70]. It can be given IV, IM, or orally, although its IV use is not approved by the United States Food and Drug Administration (FDA). It is usually given in doses of 2.5 to 10 mg. The onset of action is within 30 to 60 minutes. The dose should be decreased by one half in the elderly. Some clinicians give repeat doses as frequently as every 15 to 20 minutes in patients with severe agitation until the desired level of sedation is achieved, but according to the manufacturer doses may be repeated every 30 minutes.
• Lorazepam is commonly used due to its rapidity of action, effectiveness, short half-life, and intramuscular (IM) or intravenous (IV) route of administration [58]. The usual dose is 0.5 to 2 mg IV or IM. Some experts give doses as frequently as every 10 minutes for severely agitated patients, although standard sources of drug information suggest a dosing interval of 30 minutes. The half-life of lorazepam is 10 to 20 hours.
• Olanzapine and risperidone are the preferred medications for acutely agitated geriatric patients with dementia [82]. However, deaths have been reported following such use and the US FDA has released an advisory [83,84]. In the elderly patient, the dose for these medications should be decreased.

Thalassemia

Beta thal

• hetergenous disease


• Mutations - B+ (decreased pdc), B0 (no pdc).


• Phenotype is variable - unidentified modifying genes


• Beta-minor - B/B+ or B/B0, usually asymptomatic, microcytic (MCV<>
• Beta-intermedia -symptomatic thal but able to survive to the 2nd decade with no chronic transfusion therapy
• Beta-major - B0/B0 or B+/B+
• Diagnosis — The diagnosis of beta thalassemia minor or intermedia should be entertained in patients of any age with microcytic, hypochromic red cells. the beta thalassemias show considerable heterogeneity, patients may or may not have symptoms referable to anemia, may have variable degrees of splenomegaly and variable degrees of hemolysis.

The major differential diagnosis in such patients includes iron deficiency and the anemia of chronic inflammation, as follows:

• Patients with iron deficiency will have low levels of serum iron and ferritin and increased levels of transferrin (total iron binding capacity). A cause for blood loss will be obvious in most patients.
• Patients with the anemia of chronic inflammation will have low levels of serum iron and transferrin. Levels of ferritin will be normal or increased. An inflammatory, infectious, or malignant disease is usually the underlying cause.
• Patients with thalassemia will have normal to increased levels of serum iron and ferritin. Levels of transferrin will be normal or decreased. At least one of the patient's parents will also be affected. A family history of "iron deficiency anemia" not responding to treatment with iron is common.

The diagnosis of a beta thalassemic condition is confirmed on hemoglobin electrophoresis (table 1 and table 3). Hemoglobin A will be the major hemoglobin present. Levels of hemoglobin A2 are increased in virtually all patients, while levels of hemoglobin F are increased in about 50 percent of patients.

If hemoglobin S is present on electrophoresis along with hypochromic, microcytic red cells, and iron deficiency is absent, one of the sickle cell/thalassemia conditions is present.

• Hb A - 2 alpha, 2 beta
• Hb A2 - 2 alpha, 2 delta
• Hb F - 2 alpha and 2 gamma

Alpha thal

• 4 functional genes. two on each chromosome
• Loss of 1 - alpha thal, silent carrier.
• Loss of 2 - alpha thal minor
• Loss of 3 - alpha thal major, hemoglobin H disease. moderate degree of anemia, their red cells are microcytic, and their hemoglobin electrophoresis pattern shows 5 to 30 percent hemoglobin H (beta-4 tetramers). Chronic hemolytic anemia.
  
• Loss of 4 - hydrops fetalis

Diagnosis —

• The peripheral blood film in Hb H disease shows hypochromia and microcytosis ( readily detectable inclusion .
• Bone marrow examination reveals erythroid hyperplasia with poorly hemoglobinized erythroblasts carrying inclusion bodies.
• The diagnosis of hemoglobin H disease is confirmed by finding Hb H in circulating red cells, in concentrations from 5 to 30 percent, using a number of hemoglobin electrophoretic or chromatographic techniques (table 1 and figure 1). In addition, Hb Barts (gamma-4), a fast-moving hemoglobin, can be detected in concentrations of about 20 to 40 percent at the time of birth of a child with hemoglobin H disease [55]. This latter test has been successfully employed in California as a screening test for hemoglobin H disease [61].
• DNA-based genotyping is required for precise diagnosis, and is especially important in prenatal testing and genetic counseling (see 'Genetic counseling and antenatal diagnosis' below).

DVT therapy and prophylaxis

Prophylaxis

• 40mg clexane DAILY or 5000units of heparin BD
• TED stockings
• early mobilisation

Therapy

• 1mg/kg/BD (half-dose if renally impaired)
• Heparin requires infusion

Chest pain

DDx

• Cardiac – Angina, AMI, aortic dissection, aortis, aneursymal rupture pericarditis, myocarditis, pericardial tamponade
• Respiratory - PE, pneumonia, pneumothorax, COPD(with bullae rupture), mediastinitis
• Gastro - GORD, Ulcer, Oesophageal spasm, FB, oesophageal rupture
• Musculoskeletal - Muscle strain, Cosotochondritis, rib fracture

History:

HOPC

• When did it happen?
• What were you doing at that time?
• Describe the chest pain? Site, radiation Severity, quality, duration, Agg/relief.
• Associated symptoms.
• Chest pain/Palpitations/SOB
• Chest infections? Fever/chills/rigors. Cough/wheeze/sputum production
• Burning sensation after a heavy meal? History of heart burn?
• Recent chest trauma, muscle strains, heavy lifting
• Recent surgery, calf tenderness, immobility

Med hx

• CVD rf – smoke, drink, HT, DM, hypercholesterolemia, FH

FH

• Heart problems
• Clotting problems

O/E

Descrip

V/S- HR + regular, PR, RR, oxygen sats, temp

Cardioresp

• No peripheral signs of anemia, no clubbing, (no hepatic flap, HPOA, -ve pemberton’s sign, dupetryon’s contracture. No stigmata of infective endocarditis)
• Apex beat not displaced. No thrills or heaves. Heart sounds dual, no murmers. JVP not elevated. Carotid pulses clear. Lung bases clear. No peripheral odema. No local calf tenderness.
• Chest expansion equal&normal. No stridor. Trachea midline, not deviated. Normal to percussion. No wheeze, crackles

GIT, musculoskeletal.

“I wasn’t driven into medicine by a social conscience but by rampant curiosity” - Dr Jonathan Miller

Subdural haematoma

Patient: Fall, No LOC
CT-findings: Small dense left subdural haematoma, mass effect with sulcal obliteration with subfalcine herniation.

Findings in subdural hematoma:

1. 90% supratentorial
2. cresentic shape
3. cross suture lines.
4. does not cross dural reflections
5. acute - hyperdense, chronic - hypodense.

Definition of dynamisation

Dynamisation: The mechanical load transferred across a fracture locus can be increased, at a certain healing stage, in order to enhance bone formation, or to promote "maturation" of the healing tissues. An example would be the reduction in stiffness of an external fixation, either by loosening some clamps, reducing the number of pins, or moving the tubular construct further from the bone. Early dynamisation, i.e. before solid bridging of the bone, can result in stimulation of callus formation. The value of later dynamisation is debatable.

Pin fixators

Advantage: routine work, stabilises diaphyseal fractures, good wound access.

Disadvantages: requires reduction, limited angulatory and rotatory deformities, no axial loading permitted, high incidence of union or non-union, angulatory deformities in bone lengthing, no progressive correction allowed.

• Pin: Schanz screw/half-pin,Steinmann pin
• Clamp
• Central body
• Compression and distraction system
  

Dropping TAGs

To drop TAG below 1.7 use

1. very low fat diet
2. diet of 6-12 capsules of fish oil
3. diabetic control (esp if bad)
4. meds: fibrates/fenofibrates/nicotinic acid

Guilty conscience

Hmm I know I'll pass med school. I know I'll make a good doctor given time. But I dont feel confident enough to excel in my current exams. And if I dont, the one overwhelming feeling I would have is guilt towards my parents...then I'll hear my mummy say "Its alright you tried your best". Strange how this guilt far weighs any guilt I have towards my own inadequecies. Gotta get in my head that God controls everything that I'm merely riding a roller coaster. Arh.....Funny how though people all think I know my stuff....work!

Case - AMI & complications

Mr T, is a 64 year old gentlemen admitted to hospital 5 days ago with a cough and SOB on a b/g of a recent AMI 6 weeks ago and subsequent pleural effusion with a background history of DM.

HOPC

He first developed dry Cough and SOB 5 weeks ago. Day 1 after being discharged from hospital for his AMI. He also had fevers, sweating. No sputum production, chest pains, palpitations at that time. 4 days later he went to his GP. Had a CXR done which showed left-sided pleural effusion. Then admitted to hospital and started on oral doxycycline and amoxicillin and observed. He was subsequently discharged with the following medication. He was feeling unwell throughout. 6 days ago in the evening he suddenly developed chest pains that radiated on the left side from the front to the back. He was unable to tell whether it was of a similar nature to his previous AMI pain. There was associated coughing and SOB, no sputum production. no palpitations, nausea, vomiting or sweating. Relieved by panadeine fort and GTN. 2 days later the GP sent him to the hospital where he was managed both for his respiratory and cardiac problems. For his respiratory, had his antibiotics switched to IV ceftriaxone, U/S of the chest and CXR showed resolution of the effusion. In terms of his cardia problems, put on a holter monitor that showed a tachycardia and an abnormal rhythm. He had DC cardioversion last night and he reports feeling well and he noticed better perfusion of his fingers and better skin tone.

Had a recent AMI 6 weeks ago during the evening with symptoms of vomiting, pain to his right shoulder tip, cheeks, chest, sweating and general sense of unwell. No meleana or fresh blood, he vomited only his food contents. His pain was 4/10 chest, 6/10 left cheek and 5/10 in his right shoulder tip. It was described as a dull aching pain. No agg/reliefing factors at that time. Unable to lie in bed and had to sit in his chair and slept fitfully the rest of the night. The next day he went to the GP who sent him to the ER and was diagnosed with a AMI with raised cardiac enzymes and ECG changes. He was subsequently investigated with an angiogram and a echocardiogram. 5 days post-admission he developed a sharp pain that radiated from his shoulder to the face with no other associated symptoms. It was an 8/10 in severity. Came on suddenly and was constantly there. He was diagnosed with pericarditis. Treated with morphine and oxygen. This pain subsided 48hrs later and he was discharged.

Medical history
CVD RF: No HT, no chol, smoked a pack a week for 3 years during his university days, drinks socially, has DM.

His type II diabetes was diagnosed 5-6 years ago on routine blood screen. Currently managed on diet and exercise control. He avoids sugary food, takes low fat and lean meat. Walks his dog 4 times a week/ 30min each time. Has lost 30kg from 134-104kg. After his recent admission to hospital his blood sugars were not well controlled and was put on insulin. currently on 3 times novorapid and one evening bolus of glargine. His current average blood glucose is 6mmol/L on insulin. No macro/microvascular complications of DM.

Non-active medical conditions: gall bladder removal, recently diagnosed carpel tunnel, hayfever and asthma when he was a kid, appendicitis.

Medications:
Novorapid, glargine, ceftriaxone, fruesemide, atenolol, atorvastatin, perindopril, aspirin, clopidogrel.

FH:
Father lung cancer, 79. Mother, diabetic.

Social: Live/family, support, depresion, financial, depression, exercise/drinking/diet/smoking, insight.

Physical examination:

Peter is a well-looking man, orientated in time/place. Not in any pain or respiratory distress.
V/S: HR 60bpm, regular. RR18bpm. BP110/70. Oxygen sats on room air was 94%. On general inspection. He had no supplemental oxygen, a venous cathether in the dorsum of this right hand. Scars??

On cardiac examination:
No pale palmar creases, no manifestations of IE. On inspection of his face, no central cyanosis or jaundice. JVP was not elevated. Carotid pulse felt normal. Apex beat was not displaced. No palpable heaves or thrills. Dual heart sounds with no murmers.

On respiratory examination:
No deviation of the trachea, No palpable LN. Chest expansion was equal and normal. Stony dullness to percussion on mid to lower region on his left side. On asculation, there was decreased breath sounds and decrease vocal resonance.

In summary, Mr T is a 64 y.o gentlemen who was admitted to hosptal 5 days ago with cough and SOB on a b/g of a recent AMI. The SOB began 3 weeks ago and was treated with IV ceftriaxone. His current physical examination findings are consistent with a left sided pleural effusion. His issues are.

1. managment of his pleural effusion - which requires organized follow up with the GPs + continued Antibiotics. CXR to monitor the current pleural effusion.

2. Managment of his MI - start him on ACS medication and continue to watch for SE. and monitor complications. Optimise the control of his risk factor particularly his diabetes.

Watery diarrhoea cryptosporidium

Peter is a 47 y.o man who presents with a 4 week history of watery diarrhoea on a b/g of renal transplantation for PCKD.

HOPC:
4 weeks ago, Mr P developed a sudden episode of watery diarrhoea that has not resolved over. He has 4 diarrhoeas 8-12 times a day. No blood, mucous seen in the stool. Volume of the fecal material is high. His normal bowel motion is 1/day. He also developed fevers, chills and rigors &abdominal cramps during day 1 and 2 but has not have any of this symptoms since then.

Other relevant negatives (considering he is immunocompromised)

• No LOW, night sweats, lack of appetite.
• No cough, sputum, SOB.
• No chest pain, palpitations.
• No symptoms of UTI but has noticed a low volume of urine output (10-15mL). Claims to be dehydrated.
• No fainting, dizziness, blackouts.
• No Neurological signs.

He presented to the GP on day 2 and was subsequently admitted to hospital last week and treated.

• I- flu vaccination is up to date
• Contact - works with children (prone to norovirus, adenovirus, rotovirus diarrhoea). Last worked? No other sick contacts.
• Travel - No travel. Any dubious food? Any stream water or tank water?
• O - irrelevant
• A- lives with a cat
• D- imunnosuppressive drugs + cardiac drugs.
• Sex - never ask.

Med Hx.

1. PCKD diagnosed during the 80's. Currently on 3rd transplant. First transplant lasted 4 days. His last transplant was in 94'. On immunosupressive drugs for it. Has 1 URT infection/ 2mths. and also occasional diarrhoea. Attributed to him working with children. Hospital admissions for complications?
2. Cardiac disease with triple bypass done? any symptoms? PND, orthopnea, pillows used, exercise tol?

Medication?

Family history?

Social history?

• Live with? Family, children?
• DALYs?
• Support?
• Finanacially stable?
• depressed?
• Smokes, drink?
• exercise
• diet

Osteomyelitis

Most common bug is SA treat with flucoxicllin.
Randomly, in radical prostectomy, most commonly by pseudomonas (10-20% ciprofluxacillin resistant).

Septic arthritis

Septic arthritis - acutely inflammed joint and may destroy within 24hrs. Treat empirically with antibiotics.

Signs/symptoms

• Swollen, red joint
• associated fevers, chills and rigors, consider localised symptoms.

DDX - OA, gout, haemarthrosis, less likely psoriatic arthritis, reactive arthritis.

Ix-

1. Imaging - x-rays may be normal, consider CT, U/S, MRI.
2. FBE, ESR, CRP - raised WCC, inflammation.
3. U&E and LFT for baseline.
4. Joint aspiriate - appearance: turbid,yellow, low viscosity, microscopy: raised WCC, neutrophils. Culture& sensitivty: for the organism + sensitivity. also for polarized light microscopy: crystals (negatively bifringement crystals for gout)

Mx-

1. Analgesia
2. Empirical antibiotics until culture is known. Flucloxacillin (as most common organism is SA. consider benzylpenicillin + gentamicin)
3. Consult microbiologist
4. Consider joint wash-out especially in prosthetic knee.
5. Seek/ treat underlying cause - immunosupression? focus of infection?

Other medication to consider

1. MSSA - 1st/2nd gen cephalosporin - cephazolin/cephalexin.
2. Gp D streptococci - (like GP A but affects immunocompromised patients). Ideal medication would be penicillin as you would prefer a narrow spectrum medication to avoid antibiotic resistance (unnecessay killing of gram negative) but ceftriazone for convinience - as it is once a day dose and lower risk of PICC line occlusion.
3. infected prosthetics - combination therapy with flucoxicillin + ciprofluoxacin or rifampicin. better chance of killing organism due to presence of biofilm. options: surgery to remove joint then IV antibiotics until aseptic then joint replacement takes 9 months or lifelong prophalaxis.
4. ???Culture negative - cipro, rifampicin(treat myco), fusedic acid.

PUO: investigations

PUO is defined as a temperature of >38.3 degrees for more than 3 weeks.

DDX think broadly from top to down.

1. Infection - abscesses
2. CTD/autoimmune
3. Malignancy
4. Drugs
5. Others; hypothalamic lesion, factitious fevers.

Ix:

1. FBC - raised WCC
2. U&E - ARF, pyelonephritis, baseline for antibiotic treatment
3. LFT - liver damage especially abscess
4. Haemolytic anemia - anemia, raised weiyong is smelly bilurubin, raised urobilinogen, raised LDH, reticulocytosis, direct antiglobulin test. Considering drug reaction?
5. Myeloma screen - serum plasma electrophoresis (paraprotein & monoclonal band), urine plasma electrophoresis (Bence Jones protein). beta2 microglobulin, Ig G, M, A levels
   
6. autoimmune - Rf, ANA, dsDNA, ENA, complement activity (C3, C4), ESR, CRP, GBM, ANCA(C & P), liver/kidney microsomal antibodies.
7. peripheral blood flow cytology
8. copper, ceruloplasmin.
9. ACE
10. septic workup. consider TB.
    
11. viral serology - HIV, HAV, Hbs Ag, HCV, others:flavivirs, mycoplasma, CMV, EBV, Q fever. CD4.
12. Imaging: CT brain, body, sinuses.
    

PUO- endocarditis

Intro:
Peter is a 80 y.o gentlemen who came to the hospital via ambulance due to an episode of uncontrollable rigors and SOB. This is in the setting of a previous pacemaker infection in October 2008.

HOPC

6 days ago, he had an episode of rigors that lasted about 20min. He was at home at that time and he started shaking uncontrollably with involved all of his limbs there was associated SOB, increase RR and feeling cold. No chest pains, palpitations. There was no associated neurological deficits- muscle weakness, numbness, visual changes. There was no LOC. During this episode he called the ambulance and was sent to the hospital. He recovered in the ambulance and was feeling tired but otherwise not confused. Prior to this episode he had two similar episodes while at home and while in hospital he developed a similar episode. The total number of attacks is 4.

Patient has no recent

· Fevers ( spiking (malaria), high swinging( abscesses), constant ( gen. bacterial/ neoplasia/CTD), intermittant fever (viral especially in paediatrics) ( (has chills and rigors)
· Fatigue, LOW(despite eating a lot), night sweats.
· Localised symptoms:
1. Cough, sputum(blood? Colour? Amt?), (SOB)
2. Chest pain, palpitations, PND, orthopnea, pillows used, peripheral odema (if HF)
3. urinary – freq, urgency, nocturia, dysuria, and incontinence
4. diarrhoea, constipation, abdominal pain, blood in stools
5. Neck stiffness, photophobia, Head ache
6. Arthralgia (backpain – epidural abscess), myalgia and skin rashes.
7. ear pain, face pain (sinusitis).
8. wounds/bites.

· Dentition
· Immunization – was up to date with both his pneumococcal and flu vaccine
· Contact – no contact with anyone that’s sick recently or anyone with TB
· Travel – gone to alice springs and NT but nothing too adventurous like swimming in rivers
· Occupation – purchasing manager
· Animals – No
· Drugs – later
· Sex- Nil.

Medical conditions

· Heart failure with AF was diagnosed in 2002. He presented with APO and was unable to sleep at night his wife had to send him in ED. A pace maker was then inserted in December 2002. Since then he does not complain of PND, orthopnea, uses 1 pillow, has occasional leg swelling well controlled by diuretics. His exercise tolerance is about 50m.
· October last year he noticed a rash on his skin overlying the pacemaker. Prior to this he developed a boil on his head when he bumped his head on the shower. His GP sent him to the hospital for further investigations and he was treated for a pacemaker infection with 1/12 of antibiotic treatment and the infection was presumed cleared.
· He had no other admissions for exacerbations for HF. His current HF meds are carvedilol, spironolactone, lasix.

Non-active medical conditions
· 2 hernia operations (1980)
· Right knee replacement (80’s)
· Backpain caused by lumber sacral spinal stenosis, which is getting worse recently. Still able to drive, no muscle weakness or numbness
· OSA(04’)- used to be on CPAP but doesn’t need to use it now.
· Bilateral varicose veins

CVD risk factors – HT, high cholesterol, No DM, smoked 16 pack/yrs and quit when he was 35.

Medications-
Carvedilol, spironolactome, lasix, lipitor, irbesatan, warfarin.
Was treated on ceftriaxone, flucoxicillin and vancomycin 3 days ago for empirical treatment of sepsis.

FH- NIL
Social – live, occupation, depression, financial, support, exercise, diet.

On physical examination

· Alert, well-orientated, no signs of fevers, rigors or sweats.
· V/S – 120/80 bp, 72 HR regular, sats 98%, temperature 37.7 at 0600hrs but previously afebrile.
· CVL in for 3 days – area of insetion not oedematous or red.
· Cannula on right arm.
· Pacemaker area not oedematous, no rash.

CVD exam – normal. Looking specifically for signs of IE – Janeway, oslers, splinter haemorrhage. Petechiae in the conjunctivae. Roth spots. Splenomegaly.

Resp- Normal

Abdomen – normal

Mx issues-
Identify source of infection – septic screen - sputum, stool, urine culture. CSF? CXR. Ideally 3 samples of bloods spaced at least 30min apart.
Empirical treatment for sepsis – antibiotics ( gentamycin+ ceftapine) + supportive therapy. This treatment does not cover for gram +ve -staphs aures, enterococci. [ use ampicillin or vancomysin], TB, PCP (co-trimaxazole, if allergic to sulphur meds use pentamidine), anaerobes(metronidazole). Consider fungal causes. If less sick ceftriaxone + stat dose of gentamycin is enough.

Treatment in type II diabetes.

1. Diet/weight/exercise control
2. Oral hypoglycemics - metformin is first line. Over time additional therapy is requried. add a 2nd drug, sulfonylureas. Beware thiazolidinediones ( especailly rosiglitazone - associated fluid retention. some studies show that it is associated with coronary artery disease)
3. Consider use of alpha-glucosidase inhibitors(acarbose), lipase inhibitors (orlistat) [ not good for weight loss but indicated for glycemic control], DPP-IV inhibitors (sitagliptan (Januvia)-oral [prevents incretin break down], GLP-1 receptor agonist(exenatide (byetta)-s/c [ increases incretin levels] This new class increases insulin secretion and decreases glucagon secretion. Lowers post-prandial sugar levels and keeps pre-prandial levels low.
4. once per day insulin is added to oral hypoglycemic therapy in patients with type 2 diabetes, either insulin NPH or detemir given at bedtime or insulin glargine given in the morning or at bedtime. Start low at 10 units and vary by 10-20% over 2-4 days.
5. Total daily dose of 1unit/BMI of insulin.
   
6. Consider pre-mixed insulin or NPH + a short acting. twice a day. Not recommended in type I diabetics.
7. More complex insulin regimens are recommended when needed. Similar to type I diabetes. (long-acting basal bolus in the night+ pre-meal short or rapid acting insulin)
8. Target of 4-6mmol pre-prandial and 4-7.7 post-prandial. HbA1C of 6-7% (reflects past 3 months glucose levels)
   

ALWAYS REMEMBER PATIENT EDUCATION! insulin injections, warnings on hypoglycemia - in relation to illnesses, missed doses, exercise, diet.

Types of insulin

Ultra-short acting: insulin aspart(novorapid), insulin lispro
Onset:15min Peak: 1hr duration: 4hrs

Short-acting: actrapid, hypurin neutral
Onset:30min Peak: 4hrs duration:8hrs

Intermediate: Protaphane, Humulin NPH, Hypurin Isophane (bovine), Hypurin Isophane (porcine) via SAS.
Onset:1.5hrs Peak: 8 hrs duration: 16hrs

Long-acting: glargine(constant output), detimir
Onset: 2hrs Peak: No peak Duration: 24hrs (less for detimir)

Mixed insulin: mixtard 70/30. novomix 70/30
Both contain a short-acting(30%) and a long-acting (70%), given twice a day.

http://www.betterhealth.vic.gov.au/BHCV2/bhcarticles.nsf/pages/Diabetes_insulin_choices?OpenDocument

Managment of mucositis post chemotherapy

Mucositis

Grade I - sore but can eat/ erythamatous mucosa
Grade II - modified diet/ patchy ulceration
Grade III - unable to maintain adequete hydration/ confluent ulceration
Grade IV - cannot eat or drink/ tumor necrosis and bleeding

Mx:

1. Symptomatic topical lignocaine mixed with mylanta (use when in pain or 30 min before meal)
2. diligent mouth care for anaerobes (Na bicarbonate)
3. nystatin fungal drop - candidiasis
4. nutritional status (inflammation of mucosa) - consider nasogastric feeding or total parenteral nutrition.