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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_2738_Библиотеки_им_академика_М_И_Перельмана
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Determining cause of Cushing’s syndrome:
https://t.me/med1917
1. Serum ACTH: raised in ACTH-dependent causes
2. CRH stimulation test – if serum ACTH levels rise >35%, suggests Cushing’s
disease (<35% suggests ectopic source)
3. High dose dexamethasone suppression test (2mg QDS for 48h) = measure
0 & 48h cortisol
→ suppression = Cushing’s disease (high dose steroid = enough to suppress
pituitary adenoma cells)
→ no suppression = ectopic source (not part of endocrine axis feedback loop,
therefore not affected by negative feedback)
4. Imaging: MRI (50% pituitary adenomas = too small to detect)
5. Inferior petrosal sinus sampling if MRI is normal
Hypothalamus
CRH
Pituitary gland
Chapter 2: Endocrinology 25
Normally do CRH and high dose dexamethasone
test in combination
ACTH
Adrenal cortex
Glucocorticoids
Fig. 2.7 HPA axis.
MANAGEMENT:
1. Cushing’s disease: transsphenoidal resection of pituitary adenoma
(±radiotherapy)
2. Medical therapy to inhibit cortisol synthesis in adrenal gland
3. Adrenalectomy = last resort → will need steroid cover post-op as
endogenous levels
SUMMARY OF ADRENAL CONDITIONS:
Fig. 2.8
HYPER- HYPO-
Adrenal conditions
MCs
(aldosterone)
GCs
(cortisol)
Cushing’s CAHConn’s
Androgens
(sex hormones)
MCs & GCs
(aldosterone & cortisol)
Addison’s Secondary
• exogenous steroids
• surgically resected adrenals
• bilateral adrenal haemorrhage
Medicine
26 Chapter 2: Endocrinology
https://t.me/med1917
Thyroid disease
Hyperthyroidism
→ raised circulating thyroid hormones T3 & T4 (= thyrotoxicosis)
Signs specific to autoimmune
hyperthyroidism:
• Goitre
• Pre-tibial myxoedema
• Acropachy – swollen hands & clubbing
• Thyroid eye disease:
▶ exophthalmos – bulging eyes
▶ lagophthalmos – cannot close eyes
▶ periorbital oedema
GENERAL SYMPTOMS:
• Anxiety, irritability, insomnia
• Fatigue/weakness
• Hot/sweaty, tremor/palpitations
• Menorrhagia/diarrhoea
• Weight (but appetite)
CAUSES:
1. Autoimmune / Graves’ disease (70%) RF: P/FHx autoimmune disorders
• Autoimmune stimulation of thyroid follicular cells
• IgG autoantibodies (TRAb & TPOAb)
2. Toxic multinodular goitre (15%) RF: elderly / iodine deficient
• T3/T4 secreting nodules irresponsive to –ve feedback
3. Solitary toxic adenoma (5%)
• Benign T3/T4 secreting nodule (avg. 3mm) irresponsive to –ve feedback
4. Drug-induced: iodine, amiodarone, lithium
5. Secondary causes (rare): TSH-secreting pituitary adenoma, pregnancy
F > M
GENERAL SIGNS:
• HR/arrhythmia
• SBP
• Hyperreflexia
• ± Goitre
Thyroid function tests (TFTs):
Primary: T3/T4, TSH
Secondary: TSH, T3/T4 *
Subclinical: normal T3/T4, TSH
*Raised TSH & T3 /4 often due to
poor compliance or assay interference
Medication side-effects
Anti-thyroid drugs:
1. Rash / cholestatic jaundice
2. Agranulocytosis: infection & bleeding risk
→ FBC before Tx and monitor closely
Radioactive iodine:
= risk of hypothyroidism
Safety-netting/follow-up:
1. Signs of agranulocytosis:
= sore throat, mouth ulcer, bruising
INVESTIGATIONS:
• Hx & examination – obs, reflexes etc.
• TFTs (TSH, free T3 & T4)
• Autoantibodies (TRAb, TPOAb)
• Technetium uptake scan
▶ if no autoantibodies
MANAGEMENT:
1. Symptomatic relief: beta-blockers e.g. propranolol, bisoprolol
2. Anti-thyroid drugs: carbimazole/propylthiouracil
• Titration regimen: high dose then titrate to maintain euthyroid
• Block & replace*: maintain high dose + levothyroxine replacement
3. Radioactive iodine (
• Contraindications: pregnancy/lactation, <16y
4. Thyroidectomy: if compression Sx, malignant nodule, Tx-resistant
• Post-op complications: hypothyroidism, hypocalcaemia, vocal cord
paresis / hoarseness
Titration regimen
High dose carbimazole
(1–2m)
131
I)
HYPERTHYROIDISM
Very high dose carbimazole
▶ patchy uptake in nodules
▶ diffuse uptake in Graves’
• Assess eye disease (Graves’)
▶ visual fields / eye movements
▶ CT/MRI of orbit
HYPERthyroidism Mx needs specialist input
*Not suitable if pregnant
Block & replace
Beta-blockers
(until euthyroid)
for symptom
relief
2. Signs of thyroid crisis:
= severe HR & temp, confusion
(triggers: illness, stress, surgery, V&D)
3. Signs of tracheal compression
= SOB/stridor/dysphagia
Medicine
EUTHYROIDISM
Titrate carbimazole
Fig. 2.9
(every 4–12w)
EUTHYROIDISM
Very high dose carbimazole
+ levothyroxine replacement
(18m)
Hypothyroidism
https://t.me/med1917
→ low circulating thyroid hormones T3 & T4 (= thyrotoxicosis)
GENERAL SYMPTOMS:
• Depression/psychosis
• Slowed intellectual activity
• Fatigue/weakness
• Cold
• Amenorrhoea/constipation
• Weight
• Libido
CAUSES:
GENERAL SIGNS:
• HR
• Anaemia
• Hyporeflexia
• Dry skin
• Hair loss (outer 1/3 eyebrow)
± non-pitting oedema
± goitre
*Most common cause in UK
1. Autoimmune /Hashimoto’s thyroiditis*: RF: autoimmune disorders, 60–70s
• Autoantibodies against TPO (TPOAb)
• Gradual gland destruction: lymphocyte infiltration & fibrosis → may have
goitre
• Initial hyperthyroid state: damage releases T3/T
4
2. Primary atrophic thyroiditis:
• Autoimmune gland destruction
• Extensive lymphocyte infiltrate atrophies gland → no goitre
3. Previous hyperthyroidism treatment
• Post thyroidectomy or radioactive iodine
4. Iodine deficiency (most common cause worldwide)
5. Drug-induced: amiodarone, lithium, carbimazole, excess iodine
6. Congenital: absence/underdevelopment of thyroid gland or enzyme
deficiency
7. Postpartum thyroiditis: development within 1y of giving birth (lasts 4–6m)
8. Secondary causes (very rare): hypopituitarism
INVESTIGATIONS:
• Hx & examination – observations, reflexes, skin changes
• TFTs (TSH, free T3 & T4)
• FBC – for anaemia
• Autoantibodies (TPOAb)
Starting doses of levothyroxine:
18–49y: 50–100mcg
>50y or CVD: 25–50mcg
MANAGEMENT5:
Thyroid hormone replacement therapy: levothyroxine (T4)
• Low dose & titrate up until desired TSH levels reached
▶ review dose monthly initially, then every 3–4m
▶ review dose annually once stable
• Lifelong therapy
F > M
Chapter 2: Endocrinology 27
DDx of hypothyroidism:
• Diabetes mellitus
• Adrenal insufficiency
• Coeliac disease
• Anxiety/depression
• Dementia
Thyroid function tests (TFTs):
Primary: T3/T4, TSH
Secondary: TSH, T3/T
4
Subclinical: TSH but T3/T4 normal
Sick euthyroid syndrome: temporary TSH
during illness
Complications:
• CVD/stroke
• Dyslipidaemia
• Heart failure
• Myxoedema coma*
Patients with goitre, suspected malignancy, cardiac disease, treatment resistant or planning
a pregnancy need
5
NICE (2019) CKS: Thyroid disease
referral to endocrinologist in 2° care
*hypothermia, coma, seizures (precipitated by
another problem e.g. sepsis, stroke, HF)
Medicine
28 Chapter 2: Endocrinology
https://t.me/med1917
Goitres
DDx of goitres:
1. Physiological
2. Autoimmune: Graves’, Hashimoto’s
3. Multinodular: iodine deficiency
4. Solitary nodule: cyst, adenoma, carcinoma
Goitre classification:
0 – can’t see/feel
1 – palpable not visible
2 – visible in normal position
Epidemiology of thyroid cancer
• F:M = 3:1
• peak onset 30–50y
• RF = Asian
Prognostic factors:
• Size of tumour
• Local invasion & distant mets
• Age of patient
ASSESSMENT:
1. Hx – symptoms of compression, speed of growth, PHx radiation, FHx
2. Exam – assess size/consistency/distribution
3. Thyroid gland function – TFTs
4. USS ± aspirate – size, cystic vs. solid
5. Complications: pressure on trachea (SOB) / oesophagus (dysphagia) /
voicechange (recurrent laryngeal nerve) / thoracic inlet obstruction*
MANAGEMENT:
1. No symptoms, euthyroid &
benign: no treatment
2. If hypothyroidism: thyroxine
3. If autoimmune disease: antithyroid drugs / radioiodine / surgery
4. Surgery: if large / pressure symptoms / cosmetic / malignant
*compression of jugular vein & aorta
= causes Pemberton’s sign (facial flush if raise arms)
DIAGNOSTIC
Thyroid cancer
CLINICAL PRESENTATION:
• 90% = thyroid nodules/goitre → usually asymptomatic
• Hoarseness/dysphagia
• Thyroid dysfunction (rare)
INVESTIGATIONS:
1. Hx & examination – PHx radiation, thyroid disease, FHx
2. USS
3. FNA/biopsy – for cytology
4. Further imaging if indicated: PET / technetium scan
5. Tumour markers if cancer confirmed – thyroglobulin (+ calcitonin if
medullary cancer)
GOLD STANDARD Ix
MEN-II syndrome:
medullary thyroid carcinoma +
phaeochromocytoma +
hyperparathyroidism
Medicine
TYPES OF THYROID CANCER:
Papillary (75%) Follicular (20%) Medullary (5%) Anaplastic (rare)
Origin Follicular cells Follicular cells C cells Any cells
Features • Slow growth
• LN metastases
Who? 30–50y females 1. Sporadic = older
Prognosis Good: 80% 10y Good: 65% 10y Poor Very poor:
Well differentiated
• Slow growth
• Bone/lung
mets
• May release
calcitonin
patients
2. Part of
MEN-II syndrome
= younger
Poorly differentiated
• Fast growth
• Very invasive
• Distal mets
Elderly (M:F = 2:1)
palliative
MANAGEMENT:
1. Total thyroidectomy
2. TSH suppression – thyroxine (may need for years)
3. Follow-up – radioactive iodine (RAI) scan & tumour marker monitoring
4. Therapeutic dose of RAI if residual disease
Parathyroid disease
Serum Ca
Serum Ca
Serum Ca
intestine
https://t.me/med1917
Calcium homeostasis
1. PTH secretion if:
• Low serum Ca
• (or low vit D / high PO4)
2. PTH increases serum Ca by:
• Osteoclastic bone resorption
• Ca reabsorption in kidney
• Activating vit D in kidney
Vitamin D function: activated in kidney
1. Increase Ca absorption in gut
2. Increase osteoblastic bone formation
Calcitonin function: secreted by parafollicular (C/Chief) cells of thyroid if high
serum Ca
Hypercalcaemia (Ca >2.6mmol/L)
CAUSES:
Chapter 2: Endocrinology 29
Causes of vitamin D deficiency:
• Little sunlight
• Malabsorption
• Liver/kidney disease
Thyroid gland
Activation of Vit D
to calcitriol
)
(1,25-OH D
Small
Ca absorption
absorption
PO
4
3
PTH
Kidneys
reabsorption
Ca
calcitonin
osteoclast
activity
Bone turnover
C cell
Bones
Ca & PO
4
PTH secretion
(high PTH = Ca)
→ 1° Hyperparathyroidism e.g. adenoma
→ 2° Hyperparathyroidism e.g. long-term CKD, vit D deficient
→ 3° Hyperparathyroidism e.g. renal failure
Malignancy
( Ca = low PTH)
Vit D (calcitriol) excess
→ Breast, bronchus, kidney, prostate
→ Multiple myeloma
→ Tablets
→ Granulomatous disease e.g. sarcoid, TB
Hereditary
→ Hypocalciuric hypercalcaemia
( serum Ca, urine Ca)
Endocrine
Medication
→ Addison’s, thyrotoxicosis
→ Thiazide diuretics, lithium
SYMPTOMS:
1. Bones:
• fractures/pain
• muscle weakness
2. Stones:
• renal stones
• AKI/CKD
INVESTIGATIONS:
1. Corrected serum Ca, PTH & vit D, PO4 + U&Es
2. 24h urinary Ca: r/o familial hypercalcaemia
3. Imaging:
• DEXA scan – bone density
• Renal USS/XR – renal stones
• Localisation study – USS neck + sestamibi scan
3. Abdo groans:
• abdo pain, N&V
• constipation
• pancreatitis
4. Psychic moans:
• depression
• confusion
• consciousness
40% Ca is bound to albumin =
inactive
→ If low albumin, Ca will appear
low in tests
→ Adjust for albumin (shows
ionised calcium)
MANAGEMENT OF ACUTE SEVERE HYPERCALCAEMIA6: >3mmol/L
1. Rehydration: 0.9% saline (4–6L over 24h)
2. Loop diuretics: increase calcium excretion (only if fluid overload)
3. IV bisphosphonates if malignant (e.g. zoledronate → take 3–5d to work)
4. IV calcitonin: if aggressive presentation
Check serum Ca, U&Es, hydration status
6
Society For Endocrinology Endocrine Emergency Guidance – Emergency management of acute
hypercalcaemia in adult patients (2016)
90%
cases
Fig. 2.10 Calcium homeostasis.
Chronic 2° hyperparathyroidism causes permanent
gland activation = 3° hyperparathyroidism
Primary hyperparathyroidism
→ peak age 60y (F>M)
→ Causes:
• Single adenoma – most common
• Multiple adenomas – consider MEN-I
syndrome
→ Investigations: USS, isotope scan
→ Treatment: resection/parathyroidectomy or
calcium mimetics e.g. cinacalcet
Interpreting blood tests
PTH ALP
1° HPT High High
Malignancy Low High
triggers osmotic diuresis → DEHYDRATION
If worried about cancer: CT CAP, myeloma
screen, PSA (to find primary)
Medicine
30 Chapter 2: Endocrinology
https://t.me/med1917
Hypocalcaemia (Ca <2.2mmol/L)
CAUSES:
*Inherited disorder only affecting females
Serum calcium appears ARTIFICIALLY
LOW if do not adjust for albumin
PTH secretion
(low PTH = Ca)
→ 1° Hypoparathyroidism
e.g. post-thyroidectomy, autoimmune
→ Hypomagnesaemia = impairs PTH secretion
e.g. commonly caused by PPIs
PTH resistance
(high PTH but Ca)
Hyperphosphataemia
→ Pseudohypoparathyroidism*
= PTH receptor defect
→ CKD, rhabdomyolysis, phosphate therapy
(PO4 binds to free Ca)
Vit D deficiency
(high PTH but Ca)
Acute pancreatitis
Medication
→ Malabsorption = Crohn’s / coeliac
→ Inadequate diet / sun exposure
→ Sequestration of calcium into tissues
→ Calcitonin or bisphosphonates
SYMPTOMS:
→ Peripheral paraesthesia:
• Numbness/tingling periorally/fingers
→ Muscle cramps/spasms/tetany:
• Trousseau’s sign = claw hand with BP cuff
• Chvostek’s sign = facial nerve twitching when tapped
→ Fits/seizures/arrhythmia: if <1.9mmol/L
→ Long-term complications: depression, cataracts, bone fractures
INVESTIGATIONS:
1. Corrected serum Ca, PTH & vit D, PO
2. ECG: prolonged QT interval
4
MANAGEMENT7:
Acute mild hypocalcaemia (>1.9mmol/L):
→ Oral calcium supplements: e.g. Adcal 3, Calcichew Forte 2, Sandocal
Acute severe hypocalcaemia (≤1.9mmol/L):
→ Initial IV bolus: 10–20ml 10% calcium gluconate (in 50–100ml 5% dextrose
over 10min with ECG monitoring)
→ Followed by IV infusion: 100ml 10% calcium gluconate (in 1L normal saline or
5% dextrose over 5–10h)
→ 2nd line: oral calcium carbonate (1g TDS) + PO/IM alfacalcidol (1–2mcg)
Chronic hypocalcaemia: treat cause & monitor
→ Hypoparathyroidism: vit D supplements (calcidiol/calcitriol/alfacalcidol)
±oral calcium supplements
MEN syndrome
MEN-I MEN-IIa MEN-IIb
1. Pituitary adenoma
2. Parathyroid hyperplasia
3. Pancreatic neuroendocrine
tumour
1. Parathyroid hyperplasia
2. Medullary thyroid
carcinoma
3. Phaeochromocytoma
1. Mucosal neuromas
2. Marfanoid body habitus
3. Medullary thyroid
carcinoma
4. Phaeochromocytoma
Medicine
7
Society For Endocrinology (2016) Endocrine Emergency Guidance – Emergency management of
acute hypocalcaemia in adult patients
Sodium imbalance
https://t.me/med1917
Hypernatraemia (Na >146mmol/L)
Chapter 2: Endocrinology 31
SYMPTOMS:
• Headache
• N&V
• Lethargy/irritability/confusion
• Seizures/nystagmus
• Loss of consciousness / coma
INVESTIGATIONS/ WORK-UP:
• Fluid status
• Obs – especially BP & neuro Sx
• Medication review
• Bloods: U&Es, glucose
• Osmolality: plasma & urine
▶ Urine osm >750 suggests lack of water
▶ Urine osm <750 / lower than plasma suggests diabetes insipidus
CAUSES:
1. Low fluid intake: RFs = age >65y,
dementia, residential care
2. Diabetes insipidus: central or
nephrogenic
3. Hyperosmotic hyperglycaemic
state (HHS): osmotic diuresis =
water loss
4. Other: endocrine disorders
e.g.Conn’s, Cushing’s
MANAGEMENT:
• Rehydrate* – orally, if possible, otherwise with IV fluids
• Daily U&Es
*Reducing plasma Na too quickly can cause cerebral oedema
Hyponatraemia (Na <133mmol/L)
SYMPTOMS:
• Headache
• N&V
• Lethargy/irritability/confusion
• Seizures
• Loss of consciousness / coma
INVESTIGATIONS/ WORK-UP:
• Fluid status
• Obs – especially BP & neuro Sx
• Medication review
• Bloods: U&Es, glucose, LFT, total
protein, lipids, Ca, TFT, cortisol
• Osmolality: plasma & urine
Hypernatraemia is usually due to water
deficiency/loss rather than excess sodium
intake
Indications for urgent admission:
• Na >155 (or >146 & cannot drink)
• Neurological disturbance
• Presence of HHS
Diabetes insipidus
Central: lack of ADH secretion e.g. head injury,
pituitary tumour, pituitary surgery
Nephrogenic: renal resistance to ADH e.g. 2° to
lithium Tx / renal disease
Sx: polyuria & polydipsia
Ix: high plasma osm, low urine osm
Mx:
Central = desmopressin
Nephrogenic = salt diet, hydration, amiloride
Other Ix depend on cause:
CXR, BNP, brain MRI / CT head
DETERMINING THE CAUSE:
*SSRIs, ACEis, PPIs,
opiates, carbamazepine
Hypovolaemic
Urine
Na >30
Renal solute loss
Addison’s,
diuretics
External solute loss
Bleeds, burns, D&V,
fistula, stoma
Assess volume status
Euvolaemic
Urine
Na ≤30
glucocorticoid
deficiency, drugs*
SIADH,
Urine
Na >30
Renal failure (CKD) Heart failure
MANAGEMENT:
Hypovolaemic: IV fluids (0.9% NaCl)
Hypervolaemic: consider fluid restriction + treat underlying cause
Neurological symptoms present: IV hypertonic saline
→ PLUS review/stop causative medications
Fig. 2.11
Hypervolaemic
Urine
Na ≤30
Liver cirrhosis
Nephrotic syndrome
Pseudohyponatraemia:
Na levels appear low when very elevated lipid or
protein levels
Caution: do not correct hyponatraemia too
rapidly
→ risk of cerebral pontine myelinosis (CPM)
Medicine
https://t.me/med1917
33
https://t.me/med1917
GASTROENTEROLOGY
Clinical nutrition .....................................................................34
Gastro-oesophageal reflux disease ........................... 35
Peptic ulcer disease ...............................................................36
Gastro-intestinal haemorrhage ...................................37
Dysphagia ....................................................................................38
Oesophageal cancer .............................................................39
ABBREVIATIONS
Al – Aluminium
5-ASA – 5-aminosalicylic acid
BMI – Body mass index
BMR – Basal metabolic rate
Ca – Calcium
CBT – Cognitive behavioural therapy
CCB – Calcium channel blocker
CHO – Carbohydrate
Cr – Creatinine
CRC – Colorectal carcinoma
D&V – Diarrhoea and vomiting
DEXA – Dual-energy X-ray absorptiometry
ERCP – Endoscopic retrograde
cholangiopancreatography
FB – Foreign body
FTT – Failure to thrive
GI – Gastrointestinal
GIST – Gastrointestinal stromal tumour
GOJ – Gastro-oesophageal junction
GORD – Gastro-oesophageal reflux disease
GTN – Glyceryl trinitrate
H2RA – H2 receptor antagonist
HNPCC – Hereditary non-polyposis
colorectal cancer
IAP – Intra-abdominal pressure
IBD – Inflammatory bowel disease
IBS – Irritable bowel syndrome
IDA – Iron-deficiency anaemia
LN – Lymph node
Mg – Magnesium
MG – Myasthenia gravis
MS – Multiple sclerosis
MUAC – Mid-upper arm circumference
NAFLD – Non-alcoholic fatty liver disease
NBM – Nil by mouth
OA – Osteoarthritis
Gastric cancer ............................................................................40
Coeliac disease .........................................................................41
Obesity ...........................................................................................41
Acute diarrhoea .......................................................................42
Irritable bowel syndrome .................................................43
Inflammatory bowel disease ..........................................44
03
OGD – Oesophago-gastroduodenoscopy
PAL – Physical activity level
PBC – Primary biliary cirrhosis
PET –Positron emission tomography
PO4 – Phosphate
PPI – Proton pump inhibitor
PSC – Primary sclerosing cholangitis
PUD – Peptic ulcer disease
SI – Small intestine
SSRI – Selective serotonin reuptake
inhibitor
TCA – Tricyclic antidepressant
TIPS – Transjugular intrahepatic
portosystemic shunt
tTG – Tissue transglutaminase
UC – Ulcerative colitis
34 Chapter 3: Gastroenterology
https://t.me/med1917
Clinical nutrition
DAILY ENERGY EXPENDITURE = BMR x Stress factor x PAL
Daily fluid needs: 30–35ml/kg (2L/day)
+ 500ml per degree pyrexia
Energy composition
60% CHO (4kcal/g)
30% Fat (9kcal/g)
15% Protein (4kcal/g) = 0.8–1.5g/kg/d
Daily electrolyte requirements:
Na & K: 1mmol/kg
Ca, Mg, PO4: 0.1mmol/kg
Waist circum. in obesity
Women >88cm
Men >102cm
Albumin = poor measure of nutritional
status as drops in inflammation
Normal fold thickness
Women =30mm
Men =20mm
BMR = 1.3kcal/kg/h
= 25–30kcal/kg/d
= 2000–2500kcal/d
Assessing nutritional status
→ body composition, function &growth
1. History
• Dietary details – what, when, how much? any changes?
• Noted weight or appetite loss/change
• GI symptoms – N&V, diarrhoea, constipation, pain
• Systemic symptoms – fatigue, neurological, oedema
• Growth / FTT – in children
2. Calculate MUST score (STAMP chart in children)
3. Anthropometry
• Waist circumference & waist:hip
ratio
• Height, weight & BMI (w/h2)
• MUAC & growth charts – in
children
4. Blood tests – for specific deficiencies
• Hb, iron studies, B12 & folate – anaemia
• Urea & Cr – protein turnover / dehydration
• Core electrolytes – Na, K, Ca, Mg, PO
• ± Fat-soluble vitamins – Vitamin A, D, E (measure clotting for Vitamin K)
Surgery = 1.2
Wound/infection = 1.5
Severe burn = 2.0
• Skin fold thickness –
subcutaneous fat
• Grip strength
• Bioelectric impedance/DEXA –
body composition
4
BMR = Basal metabolic rate
PAL = Physical activity level
Bed-bound = 1.2
Light activity = 1.5
Moderate activity = 1.8
High activity = 2.2
Enteral tube Indications Complications/disadvantages
NG tube
(nasogastric)
NJ tube
(nasojejunal)
PEG/RIG tube
(percutaneous)
STEPWISE APPROACH to nutritional support:
DIET ADVICE
FOOD FORTIFICATION
ORAL SUPPLEMENTS
PAR-/ENTERAL FEEDING
Medicine
Nutritional support
• Poor dentition/oral pathology
• Inflamed mucosa (chemo/candidiasis)
• Swallow problems (stroke/MND)
• Aspiration risk ( GCS, laryngeal ner ve palsy)
• Obstructing stricture (cancer, radiotherapy)
• Aspiration of stomach contents (bowel obstruction)
• Severe vomiting (e.g. hyperemesis gravidarum)
• Gastric cancer, causing outlet obstruction
• Gastroparesis (in diabetes)
• Pancreatic cancer, causing duodenal obstruction
• More comfortable on pharynx/oesophagus
• Avoid nasal erosion
• If longer term nutrition needed (>4m)
e.g. stroke with poor swallow, throat cancer
PARENTERAL FEEDING:
Indications:
• Shortened bowel with high output
stoma
• Dysfunctional bowel e.g. ileus, colitis
• Contraindicated for enteral feeding
e.g. no access
• Need to replace trace elements:
vitamins & minerals
• Displaced by coughing/vomiting
(check position via CXR)
• Misplaced tube (into lung)
(pneumothorax, pneumonia, death)
• Need more complex, pre-digested formula
• Require radiological/endoscopic placement
• Less likely to displace
(can send patients home with them)
• Cannot remove if been inserted <6w
(tube tract not yet healed so complications)
• Needs radiological/endoscopic placement
• Stoma complications
Complications
→ Infection of access site
→ Venous thrombosis
Metabolic complications:
→ Higher level of bone turnover (causes
osteoporosis)
→ Associated liver dysfunction (check LFTs)
→ Risk of over- or under-hydration
Remove if:
1. Displaced
2. Recovered
3. >6w
Must monitor
FBC, U&Es, LFT,
bone profile &
magnesium
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