Monday, August 14, 2006

Final FRCA part 1

Acute Pain management:
Acute pain---spectrum---Chronic pain
May not fit exactly in one group
Scope of acute pain services increasing
Neuropathic pain can present within hours- as acute pain
Certain surgeries more prone to develop chronic pain- link between acute post-op pain and chronic pain. Potentiation of dorsal horn neurones in acute situation if persists longer- chronic pain.
Study of 5000 chronic pain patients- 22.5% were due to surgery, 17.5% were trauma related.
Complications of severe post op acute pain-
Epidural- reduces all these risks
Pain medicine is gaining special interest

Dead Space measurement:
A Invasive
B Non-invasive
a. SBT-CO2 (Fowler’s)
b. Bohr’s
c. Bohr-Enghoff
d. Kouloris/Romero method

a. Fowler’s - Single breath technique using CO2 measurement- FCO2 plotted against expired volume. Three phases of graph obtained. Phase 1- airway deadspace, 2- interface between airway/alveolar space mixing, 3-alveolar gas expired.
Midpoint of phase 2 by Fowler’s method will give anatomical Vd. 85ml in intubated pt, it is diffusive boundry, so varies with breath holding, end-inspiratory pause.
Phase 3 slope- upward (causes- i. well ventilated units empty first (mixed with N), ill ventilated ones empty later- pure CO2; ii. More CO2 keeps coming into lung from circulation as expiration continues)
PE- normal slope, but large VD
R-L shunt-- normal slope, but large VD
Intrapulmonary shunting- steep phase 3, large Vd.

b. Bohr’s - Assuming that last part of expirate represents alveolar air- Bohr’s deadspace can be calculated.

c. PaCO2 in ABG can be used to calculate the FCO2 of alveolar gas in equilibrium with arterial blood. This FCO2 value can be used in dead space equation- Bohr-Enghoff equation.

d. Kouloris/Romero method- non-invasive, combines impairment of CO2 elimination by airway and alveolar deadspaces.

Bohr-Enghoff method- Only simple clinical method where Vd increases with increasing severity of V/Q mismatch.
Diagrams- SBT_CO2, Kouloris/Romero Vd

Fluid absorption in endoscopic surgery-

Fluids used-
Glycine 1.5%
Mannitol
Sorbitol
NS
Sterile water

Surgeries performed-
TURP
TURBT
TCRE
Cystoscopy
Arthroscopy
Renal stone surgery
Rectal tumour
Vesical ultrasonic lithotripsy

Mechanism of fluid absorption-
Absorption- if irrigation fluid pressure more than 1.5 Kpa- TURP, TCRE
Extravagation- intra/extra peritoneal- renal stone surgery

Risk factors-
Smoking
Prostate cancer= benign disease
Extent of resection
Duration
Capsular perforation
Damage to venous sinuses
Fibroid resection in TCRE

Incidence-
1-8% mild to moderate TURS
Identification method (definition of TURS) affects incidence-
i. severity score- 1, 2, 3, CVS/CNS symptoms
ii. intra-op/post-op symptoms Vs amount of fluid absorbed

Symptoms-
Prickling sensation
Restless
Headache
Bradycardia
Hypotension
Feeling bad
Chest pain
Nausea
Vomiting
Poor UOP
Vision disturbed
HT
Reduced LOC
Diarrhoea
Abd pain
Confusion
Coma
Death

Severe TURS
CNS-92%
CVS-54%
Eye-42%
GIT- 25%
ARF- 21%
Death-25%

PK & PD-

Glycine-
Non-essential aa
0.3 mmol/l
Cheap, non allergic
T1/2 distri- 6 min
T1/2 elim 40 min-hours- dose dependent
BBB restricted
Liver metabolism- ammonia, 5-10% unchanged in urine
Osmotic diuresis

5-8 mmol/l visual disturbance
>10 N V
20-80 fatal

Mannitol
Glucose isomer
3 & 5%
Short distri T1/2
T ½ el 100 min
100 unchanged in urine
Osmotic diuresis
0.5-1% solution not diuretic
Few or no symptoms on absorption into circulation

Sorbitol
T1/2 dist 6 min
T1/2 el 33 min
Glucose+ fructose
Sorbitol- no reports of TURS
Sorbitol+mannitol- five case reports

Plasma dilution mannitol>mannitol+sorbitol> glycine 1.5%
Sorbitol & glycine enter cells and absorb water by osmosis- IV dehydration, cell swelling.

Pathophysiology

Haemodynamics- transient raised CVP, SOB, pulmonary edema, then hpokinetic haemodynamics phase- brady, hypovol, hypotension, reduced CO.

Heart- brady, ST-T depression, reduced conductivity, collapse

Blood- Reduced proteins, Na, osmolality, PaO2; increased K, urosepsis.

Brain- depression due to edema, Ammonia (>100micromol/l) glycolic acid, glyoxilic acid, glutamate, hyperglycinaemia; cerebral herniation
NS- >50 ml/kg absorption- few CNS symptoms.
Mannitol- ok
Sorbitol- fructose intolerance, lactic acidosis, enceph in presence of liver failure.

Kidney- diuresis, natriuresis, hpotension, urosepsis- renal infaction due to hypoperfusion, Increased ADH

Extravagation
ECF dissolves in this fluid, hyponatraemia, brady, hypovol, hypotension, reduced CO


Comparisons
Animal studies- glycine worst outcome
Volunteers-More CVS/CNS symptoms with glycine than other 2
Clinical- Glycine 1% = 1.5% more symptoms like nausea than mannitol; for CVS all = but > than mannitol+sorbitol


Measurement of fluid absorption-
Serum Na- repeated measurements, practical difficulty
Volumetric fluid balance- input+ output; practically difficult- but good to detect extravagation
Gravimetry- theatre table with facility to weigh patient
CVP- transient rise, so not useful; >500ml absorption in <10 min for change.
Isotope measurement- safety issue
Ethanol- similar to Isotope measurement, 1% ethanol
Sensitivity 75ml/10 min of surgery.
If > 75ml/10 min of surgery- increased absorption

Extravagation- Gravimetry, Volumetric fluid balance; other methods late detection- 15-20 min

Prevention-
Surgeon education
Duration
Lower fluid bag-60 cm
Low pressure irrigation- bladder canula suprapubically or special port in resectoscope to keep fluid draining
Alternate techniques- bipolar resectoscope, vaporisation
Drugs- vasoconstrictors, harmoes for rndometrial size reduction

Treatment-
Vision- spontaneous resolution
N, V- antiemetics
CVS support- atropine, Ca, fluid replacement if hypovolaemia, hypotension
Hypertonic saline if Na < 120 mmol/l, evidence based.
Raise Na by 1mmol/l/hr
Frusemide- only if pulmonary edema and spont diuresis doesn’t occur, not routinely.

Extravagation-
Same as above + may need surgery- will remove electrolyte- Hypertonic saline required.

Monday, August 07, 2006

Glutamine for ITU nutrition

www.medicineteacher.blogspot.com

Functions glutamine

Glutamine becomes an essential amino acid in the human body during times of stress including critical illness and after major trauma or surgery.

Glutamine is the most abundant free amino acid in the extracellular and intracellular compartments, contributing to more than 50% of the body

s free amino acid pool (Young 2001).

Function Cont.

Supports rapidly proliferating cells, such as lymphocytes and enterocytes
à important to immune and intestinal integrity.

Acid-base homeostasis.

Nitrogen and ammonium carrier.

Glutamine levels during illness

ICU patient mortality has been shown to be significantly higher for patients with low plasma glutamine levels

(Oudemans-van Staaten, et al. 2001).

Animal studies

Predominantly rat studies have showed that glutamine:

Limits intestinal permeability

Reduces gut atrophy

Preserves intestinal and extraintestinal IgA levels

Decreases intestinal proinflammatory cytokine production

Early human research on glutamine

Many researchers have studied replacement of glutamine, either parenterally or enterally, assuming this could lead to improved patient outcomes.

Until 2003, published trials were small: each enrolled between 35 to 84 patients.

Some studies suggested lower infection rates and perhaps improved mortality.

A meta-analysis by Novak et al. (2002) showed inconclusive results. Parenteral glutamine showed a trend towards reduced mortality as well as fewer infectious complications but no reduction in length of stay.

Enteral Glutamine

Hall et al. (2003): prospective, triple blinded study in a 10 bed ICU in Perth, Australia.

363 patients; 20g/day enteral glutamine.

No difference in: mortality at 6 months
severe sepsis
infections
consumption of inotropes.

Enteral Glutamine Cont.

Schulman et al. (2005): prospective, unblinded study involving 185 patients admitted to a surgical and trauma ICU in Charlottesville, Virginia, USA.

Patients were sequentially assigned to either standard enteral feeds or 20-40g/day glutamine supplemented feeds.

No significant difference in in-hospital mortality or secondary end points (there was a trend towards higher mortality in the glutamine group).

Why no benefit with enteral glutamine?

The proposed benefit of glutamine for human cells may also extend to bacteria.

Animal studies have demonstrated an increased growth rate of bacteria when incubated in the presence of glutamine.

(Kajikawa 2002).

Parenteral Glutamine

Dechelotte P: French study involving 114 patients in 16 ICUs.

Prospective, double-blind, controlled, randomized trial.

Received 0.5g/kg/day glutamine parenterally.

infection rate: 0.45 vs 0.71 infections per patient (p <>

pneumonia: 10 vs 19 patients (p <>

hyperglycaemia: 20 vs 30 patients (p <>

Early death rate and 6-month survival were not different.
Survivors at 6 months: glutamine group 72%, control 83%.

Have the studies been
giving enough glutamine?

Most naturally occurring food proteins contain 4-8% of their amino acid residues as glutamine; hence, the daily consumption of glutamine is usually less than 10g. The optimal dose of glutamine is unknown

(Hall et al. 2003).

What about glutamine use
in other areas of medicine

?

Studies in:

Premature infants

Bone marrow transplants

Inflammatory bowel disease

Show similar lack of benefit.

Costs

Glutamine 10g 50ml bag

£15.96
Glutamine 20g 100ml bag
£

29.60

Kabiven 9 bag

£

31.75

Last year, Ysbyty Gwynedd spent

£

12 000 on Kabiven 9.

Therefore adding 20g of glutamine would almost double the cost of enteral feeding.

Conclusions

There is insufficient evidence to conclusively determine whether glutamine supplementation for ICU patients is beneficial.

The best evidence so far indicates that there is likely to be no benefit.

The additional cost can not be justified.

References

Dechelotte P, Hasselmann M, Cynober L, et al. L-alanyl-L-glutamine dipeptide supplemented total parenteral nutrition reduces infectious complications and glucose intolerance in critically ill patients: The French controlled, randomized, double-blind, multicenter study. Crit Care Med 2006;34:598-604.

Hall JC, Dobb G, Hall J, de Sousa R, Brennan L, McCauley R: A prospective randomized trail of enteral glutamine in critical illness 2003;29:1710-1716.

Kajikawa H, Mitsumori M, Ohmomo S: Stimulatory and inhibitory effects of protein amino acids on growth rate and efficiency of mixed ruminal bacteria. J Diary Sci 2002;85:2015-2022.

Oudemans-van Staaten HM, Bosman RJ, Treskes M, et al: Plasma glutamine depletion and patient outcome in acute ICU admissions. Intensive Care Med 2001; 27:84-90.

Novak F, Heyland DK, Avenell A, et al: Glutamine supplementation in serious illness: A systematic review of the evidence. Crit Care Med 2002; 30:2022-2029.

Schulman AS, Willcutts KF, Claridge JA, et al. Does the addition of glutamine to enteral feeds affect patient mortality?. Crit Care Med 2005 Vol. 33, No. 11.

Young VR, Ajami AM. Glutamine: The emperor or his clothes? J Nutr 2001; 131(9 Suppl):2449S-2459S.

The End. Thank you.

Thursday, August 03, 2006

Addison's disease

Addison’s disease

Addison’s
Glucocorticoid deficiency
Mineralocoeticoid deficiency usually
Primary, secondary
Acute, chronic, acute on chronic
Autoimmune mostly

clinically
Low BM
Postural hypotension
N V D weight loss
Pigmentation
Reduced hair
May not be obvious until stressed
Reduced calcium very rare

lab
Low Na, high K & urea
Low BM
Elevated ACTH
SST- 250 microgram, 0, 30, 60 min cortisol level, >580 ug excludes diagnosis
Reduced renin activity
Reduced aldosterone

adrenal crisis
Precipitated by stress
Hypotension, low Na, High K, low BM
Can present similar to septic shock
Hypovolaemic picture

treatment
ITU
Hydrocortisone 200 mg stat, 100 mg qds
Fluid resuscitation
Glucose resuscitation
Inotropes
Dexamethasone if diagnosis not clear, as doesn’t interfere with cortisol level.

hypercalcaemia
Increased bone resorption
Hyperparathyroidism
Malignancy- metastasis, PTH like peptides, lymphoma, mm
Paget’s disease
Immobilisation
Increased GIT abs-
Intake- milk alkalli, antacids, Ca
Excess Vit D- vit D, TB, sarcoidosis, lymphoma
Decreased Output-
Renal failure
Thiazides
FHH