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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_5230_Библиотеки_им_академика_М_И_Перельмана.pdf
Gilbert’s syndrome
$ Benign autosomal recessive disease causing mild, self- resolving
unconjugated hyperbilirubinaemia typically during acute illness.
Choledocholithiasis
$ Gallstone in common bile duct, causing obstructive jaundice.
Risk factors ♀, pregnancy, DM, obesity,age; Symptoms Often none, pre-
ceding biliary colic, dark urine, pale stool;
tenderness;
Treatment Maintain hydration, exclude pancreatitis and cholangitis,
Investigations blds iALP, ibilirubin; USS Dilated bile ducts;
Signs Jaundice, mild RUQ
prophylactic antibiotics (eg co- amoxiclav .2g/ 8h IV); ERCP permits diagnosis and stone removal; cholecystectomy usually deferred until jaundice
resolved;
Complications Pancreatitis, cholangitis, hepatitis, clotting defects.
Cholangitis
$ Infection of the bile duct with Charcot’s triad:fever, jaundice, RUQ pain.
Symptoms Unwell, abdo pain, rigors, jaundice; Signs itemp, iHR ±dB P,
RUQ tenderness (Murphy ’s +ve);
ibilirubin;
USS ?duct dilatation, stones; Treatment Eg co- amoxiclav .2g/
Investigations blds iWCC, iCRP,
8h IV; may need an urgent ERCP if gallstones are in the common bileduct.
Primary biliary cholangitis(E OHCM1p. 278.)
$ Chronic, progressive autoimmune destruction of interlobular bile
ducts. Previously known as primary biliary cirrhosis.
Symptoms and signs Fatigue, pruritus, cholestatic jaundice, cirrhosis; Investigations blds iALP, iγGT ±ibilirubin, iIgM, anti- mitochondrial antibodies (E
p. 330);
USS±liver biopsy for staging; TreatmentUrsodeoxycholic acid (helps
symptoms and delays progression); colestyramine 4– 8g/ 24h PO for itching;
monitor for signs of decompensation and screen for osteoporosis (DEXA);
in advanced disease immunosuppression (eg methotrexate, steroids); replace
fat- soluble vitamins (A, D, E, K); refer for liver transplant assessment.
Primary sclerosing cholangitis(E OHCM1p. 278.)
$ Inammation and brosis of intra- and extrahepatic bileducts.
Symptoms and signs Chronic biliary obstruction leading to cirrhosis; IBD
present in 780%, of which 790% UC, but course of IBD not related
to PSC;
Investigations blds iALP, ±ibilirubin, iimmunoglobulin levels,
antismooth muscle antibodies (SMA), ANA, p- ANCA, HLA- A, B8
orDR3;
ERCPMultiple strictures; brosis on liver biopsy; TreatmentTrials of
immunosuppressive agents have proven disappointing; ursodeoxycholic
acid can help symptoms; screen for osteoporosis (DEXA) and monitor
for cholangiocarcinoma (7% per annum); transplantation key, but disease
recurs in 5% post transplant.
Cholangiocarcinoma(OHCM1 Ep. 282.)
$ Adenocarcinoma (90%) or squamous cell carcinoma of intra- and
extrahepatic biliary epithelium; strong relationship with IBD andPSC.
Symptoms and signsJaundice, pruritus, weight loss, dull RUQache. Courvoisier’s
An enlarged gallbladder in the presence of jaundice is not caused by
law
gallstones (suggests pancreatic or biliary cancer);
ibilirubin, CA9.9;
USS, MRCP, ERCP± biopsy; Treatment Surgery (0– 40%);
Investigations blds iALP,
else palliate:chemotherapy, ERCP + stenting.
333JAUNDICE
Chapter
Endocrinology
2Hypoglycaemia emergency 336
Hypoglycaemia 337
2Hyperglycaemia emergency 338
Hyperglycaemia 340
Diabetes mellitus 342
Pituitary axis 345
Adrenal disease 346
Thyroid disease 348
335
336 CHAPTER Endocrinology
2Hypoglycaemia emergency
2 Airway
2 Breathing
2 Circulation
2 Disability
2 Exposure
Check airway is patent; consider manoeuvres/ adjuncts
If no respiratory eort—
If no palpable pulse—
If GCS ≤8—
Check for insulin pump and detach if present
CALL ANAESTHETIST
CALL ARREST TEAM
CALL ARREST TEAM
3Call for senior help early if patient deteriorating.
• Blood glucose is normally >4mmol/ L (‘four is the oor’)
• Poorly controlled diabetics can have symptoms of hypoglycaemia
with a glucose >3.5mmol/ L.
Coma or low GCS withlow glucose
• Begin to follow emergency protocol E pp. 352–3 (lowGCS)
• Protectairway: simple airway manoeuvres/adjuncts
•
5L/ min O
• Establish
• Give
if SOB or sats<94%
2
venous access unless already present
IV glucose STAT (75– 00mL of 20% or 200mL of0%)
• If unable to establish IV access, or for large insulin overdoses give mg
glucagonSC/ IM
• If hypoglycaemia is responsible, GCS should return to 5 in<0min
• Start
L 0% glucose/ 4– 8h IV, adjust rate to keep glucose >5mmol/ L
•
Monitor nger- prick glucose every 30min until patientstable
• Attempt to determine the
cause of the hypoglycaemia and review
diabetes treatment if appropriate
• Call for
seniorhelp
• Reassess, starting with A, B, C; if no improvement Epp. 352–3.
GCS 5/ 5 withlow glucose
• Give 5– 20g of quick- acting carbohydrate (eg. 70– 225mL
Lucozade
•
Monitor nger- prick glucose hourly until stable, aim for >5mmol/ L
®
) or one glucose gel (eg GlucoGel®)orally
• If CBG remains <4.0mmol/ L despite 3× oral glucose, consider
glucagon or IV glucose as above mentioned
• Once the patient has recovered, give a long- acting carbohydrate
(egtoast, biscuits)
• Attempt to determine the
cause of the hypoglycaemia (Box .)
andadjust diabetes treatment as appropriate.
2Box . Causes ofhypoglycaemia
• Insulin overdose (may be iatrogenic)
• Medication (eg sulfonylurea)
• Fasting/ starvation
• Sepsis
• Renal failure
Insulin pumps deliver continuous fast or short-acting insulin via a subcutaneous cannula which can
be removed to stop the infusion in a hypoglycaemic emergency.
• Alcoholexcess
• Acute liver failure
• Insulinoma
• Glucocorticoid deficiency
• Neoplasm.
Hypoglycaemia
2Worrying features dGCS, recurrent episodes, loss of awareness2,
non- diabetic, lacking insight, or unable to communicate symptoms.
Think about Most likelyExcess insulin or oral hypoglycaemics in a dia-
betic or accidental dose in non- diabetic, alcohol;
(DM or post- gastric surgery), liver failure, adrenal failure (Addison’s), pituitary insuciency, sepsis, insulinoma, other neoplasia, malaria.
Ask about Sweating, hunger, exercise, recent food, previous hypos
and awareness
ness, anxiety, palpitations;
crine disease;
SHAlcohol, occupation (eg commercial driver).
2
, usual blood sugars, seizures, weight loss, tired-
DH Insulin dose, oral hypoglycaemic dose, compliance;
PMH DM, gastric surgery, liver or endo-
ObsHR, BP, RR, temp, GCS, recent and current blood glucose.
Look forPale, sweating, tremor, slurred speech, focal neurology (can be se-
vere, eg hemiplegia), dGCS, abdo scars (injection sites, lipodystrophy), insulin
pump (detach if present), pigmented scars, jaundice, spider naevi, hepatomegaly.
Investigations Finger- prick glucose Use a clean finger. If the result is un-
expected ask for a repeat on a dierent machine and send a blood sample
in a fluoride oxalate (E p. 545) tube for a laboratory glucose result. If
known to be diabetic
send samples for FBC, U+E, LFT, glucose, insulin, Cpeptide, and cortisol, prior to correcting hypoglycaemia; do not let this delay
treatment.
Further investigationsHypoglycaemia is very rare in an otherwise
healthy non- diabetic patient in the absence of alcohol. Consider ‘other’
causes listed previously (also see Box .2). For suspected insulinoma, the
investigation of choice is glucose, insulin, and C- peptide levels at the time
of hypoglycaemia or after a 72h observed fast. See E OHCMp. 209.
Treatment Follow treatment for ‘Hypoglycaemia emergency’ (E p. 336).
DM
A single episode of mild hypoglycaemia does not need change of medication. If patient having regular hypos, consider diurnal pattern of hypos, consider
diurnal pattern of hypos, and consider reduction of appropriate insulin dose
by 20%; consult BNF to reduce doses of oral hypoglycaemics. Ensure patient is
aware of sick day rules (E Box .8).
Alcohol
will not reoccur after correction in absence of further alcohol consumption.
Once blood sugars are stable patient can be discharged.
Fast passage of food into small intestine (following gastric surgery or in diabetic
autonomic neuropathy) can cause fluid shifts and rapid glucose absorption.
Excessive insulin secretion results in rebound hypoglycaemia – 3h after meal.
Adiet low in glucose and high in fibre improves symptoms. Aim for frequent,
smaller meals.
Neoplasia
If suspected, arrange appropriate imaging and referral.
I Box .2 Hypoglycaemia covered elsewhere
Addison’s E p. 345, p. 346 Sepsis E p. 485
Acute liver failure E p. 328 Pituitary failure E p. 345
2
Loss of earl y autonomic symptoms warning of mild h ypoglycaemia (eg tremor, sweating) seen in
those with longstanding DM and frequent hypoglycaemic episodes.
OtherDumping syndrome
not
Hypoglycaemia following alcohol
Dumping syndrome
337HYPOGLYCAEMIA
338 CHAPTER Endocrinology
2Hyperglycaemia emergency
2 Airway
2 Breathing
2 Circulation
2 Disability
2 Exposure
Check airway is patent; consider manoeuvres/ adjuncts
If no respiratory eort—
If no palpable pulse—
If GCS ≤8—
Look for cause
CALL RAPID RESPONSE TEAM
CALL ARREST TEAM
CALL ARREST TEAM
3Call for senior help early.
Diabetic ketoacidosis (DKA)
Suspect DKA3 in any patient with known diabetes or new hyperglycaemia who is unwell, vomiting, or has abdominal pain. Do venous blood
gases (VBG) as well as finger-prick glucose
2Diagnosis
• Acidaemia (venous pH <7.3 or HCO
• Ketonaemia (capillary ketones >3mmol/L or urine ketones ≥2+)
and ketones for all patients.
–
<5mmol)
3
• Hyperglycaemia (blood glucose >.0mmol/L).
5L/min O if SOB or sats <94%
•
• Establish venous access, take bloods:
•
VBG, FBC, U+E, glucose, osmolality, HCO
•
Replace volume and correct electrolytes (caution in cardiac failure);
•
if SBP <90mmHg, give 500mL 0.9% saline IV over 0– 5min then
recheck; if SBP <90, give further
5min and call ICU/ critical careteams
•
if SBP ≥90, give L 0.9% saline IV over60min
•
after initial boluses, replace K+ in fluids if <5.5mmol/L. If K+
500mL 0.9% saline IV over 0–
3.5–5.5mmol/L add 40mmol per litre NaCl,
−
, blood cultures
3
+
if K
<3.5 mmol/L
seek critical care input
•
Replace insulin Start a fixed rate insulin infusion of 0.unit/ kg/ h IV (use
50units human soluble insulin eg Actrapid
®
in 50mL 0.9% saline; max
rate 5units/ h). Continue patient’s long-acting insulin.
•
Monitor fluid status, finger- prick glucose, and ketones hourly. Check
VBG at 60min then 2hrly thereafter. Monitor U+E 4hrly. Consider
catheter to monitor fluid output. Aim for fall in ketones 0.5mmol/L/h,
rise in HCO
•
Prevent hypoglycaemia When blood glucose is <4mmol/L start 0%
−
of 3mmol/L/h, or fall in glucose 3mmol/L/h (Box .3)
3
glucose 25mL/h alongside fluids; consider slowing insulin to 0.05units/kg/h
•
Look for cause CRP, ECG, CXR, MSU, blood cultures
•
Reassess starting with A, B, C… (Box .4).
2Box .3 Consider HDU admission inDKAfor
• Ketones >6mmol
• GCS <2, sats<92%
• SBP <90mmHg
• Young people, elderly, comorbidities, or pregnant
−
• HCO
<5mmol/ L, pH<7.
3
+
• K
<3.5mmol/ L, anion gap >6 E p. 63
339HYPERGLYCAEMIA EMERGENCY
Hyperosmolar hyperglycaemic state (HHS)
Typically unwell patients with T2DM.
6
Occurs over days to weeks. Look
for dehydration, marked hyperglycaemia ≥30mmol/L, serum osmolality
≥320mosmol/kg, ketones <3mmol/L.
•
5L/min O if SOB or sats <94%
• Establish
•
venous access, take bloods:
•
FBC, U+E, glucose, serum osmolality,7 blood cultures
Replace uid:
•
Give L 0.9% saline over 60min
•
Give sustained fluid resuscitation and monitor fluid status (a guide
for adults would be L over 2h, L over 4h, L over 4h, L over 8h).
Most patients have deficit >8L.
•
Caution in elderly patients, heart failure, or renal impairment
•
Correct electrolytes:
•
if K+ 3.5–5.5mmol/L add 40mmol per litre NaCL
•
if K+ <3.5mmol/L seek critical care input
•
if Na+ >60mmol/L seek senior help
•
Start IV insulin (fixed rate at 0.05units/ kg/ h) ONLY if plasma ketones
>mmol/ L or ≥2+ urinary ketones OR glucose, fails to fall with fluid
resuscitation alone (use 50units human soluble insulin eg Actrapid
®
in
50mL 0.9% saline)
•
Monitor fluid status, finger- prick glucose, and ketones (if elevated
hourly. Check VBG 2–4hrly. Consider catheter to monitor
initially)
fluid output. Aim for fall in blood glucose 4–6mmol/L/h
•
Look for cause CRP, ECG, CXR, MSU
•
Reassess starting with A, B, C. . .(Box .4)
• For complications of DKA/HHS, see Box .5.
2Box .4 Precipitants of DKA/HHS
• Infection
• MI
• Poor compliance
• Stroke
• Trauma/ surgery
• Pancreatitis
• SGLT2 inhibitors (euglycaemic DKA)
• Pregnancy.
2Box .5 Complications of DKA/HHS
• Cerebral oedema (seek help if GCS drops)
• VTE (give LMWH unless contraindicated)
• Hypokalaemia
• Foot ulceration (check and protect pressure areas, especially if
For Joint British Diabetes Societies guidelines see Mhttps://abcd.care/resource/
management-diabetic-ketoacidosis-dka-adults
Blood glucose may be normal in some patients, especially those taking SGLT2 inhibitors.
On the ward, give IV potassium no faster than 0mmol/h. Faster rates of infusion require moni-
toring which is usually only available on HDU/ITU.
For Joint British Diabetes Societies guidelines see Mhttps://abcd.care/resource/
management-hyperosmolar-hyperglycaemic-state-hhs
Plasma osmolality may be estimated as 2×([Na
lab measurement.
On the ward, give IV potassium no faster than 0mmol/h.
+
] + [K+])+ urea + glucose while awaiting a formal
↓
GCS.
340 CHAPTER Endocrinology
Hyperglycaemia
2Worrying features dGCS, ketonuria, acidosis, vomiting.
Think about 2Emergencies Diabetic ketoacidosis (DKA E p. 34),
hyperosmolar hyperglycaemic state (HHS E p. 34);DKA takes hours
to days to develop while HHS takes days toweeks.
food, steroids, non- compliance with diabetic treatment, infection, or acute
illness (in diabetics or severely unwell non- diabetics), new diagnosisofDM.
Ask about‘Osmotic symptoms’ (thirst, polyuria, frequency, urgency),
tiredness, weight loss, vomiting, rashes, breathlessness, cough, sputum,
chest pain, abdo pain, dysuria;
PMHDM;DHInsulin dose, oral hypogly-
caemic dose, medication changes and compliance, steroids;
Obs Temp, RR, GCS, urine dip, BM, recent and current blood glucose,
fluid balance.
Look forVolume status (E p. 402), sweet- smelling breath (ketones);Signs
Check skin thoroughly (including perineum and feet) for abscesses
ofinfection
or rashes and injection site problems, look in mouth for dental infection, chest
for poor air entry or creps, abdominal tenderness.
Investigations Finger- prick glucose (±ketones if available and sus-
pect DKA) repeat if result unexpected;
dence of infection (E pp. 68–9);
blds Send if patient is unwell, has
persistent hyperglycaemia (over 48h), or has urinary ketones (TDM),
request FBC, U+E, LFT, osmolality, pH/ HCO
tures;
ABG Unnecessary unless concerns regarding respiratory status
(venous pH adequate for DKA);
ECG/ CXRIf treatment has been required.
Treatment A single episode of hyperglycaemia in an otherwise well
patient is unlikely to suggest underlying pathology.
Type diabetes Check finger- prick glucose (+ ketones if available) and
urine. Glucose is usually high in DKA but may be transiently normal soon
after a dose of insulin. Assess volume status (E p. 402), check dipstick
for ketonuria and check a VBG for pH/ HCO
sence of urinary ketones excludes DKA). If hyperglycaemia persists, try
to establish any diurnal pattern and i appropriate insulin doses by 20%
with close monitoring of blood glucose.
Type 2 diabetes Check finger- prick glucose and urine. Blood glucose is
usually >30mmol/L in HHS, measure serum osmolality if HHS suspected. Monitor glucose levels every 6h for 48h, increase oral/ IV fluid
intake, and reassess. DKA can occur in type 2 diabetics who require insulin but it is very unusual (even low levels of residual insulin production
inhibit ketogenesis). For persistent hyperglycaemia increase the dose of
hypoglycaemic medication or consider starting/ increasing insulin with
frequent finger- prick glucose checks.
For all diabetic patients with blood glucose >2mmol/L who are unable to
eat and drink (eg due to surgery or acute illness) consider starting variable rate intravenous insulin infusion (‘sliding scales’ E p. 34).
CommonAfter sugary
Urine dipstick Ketones, evi-
–
(venous), blood cul-
3
−
(normal venous pH or ab-
3
SHAlcohol.
Diabetic ketoacidosis (DKA)(E p. 338.)
K Insulin deficiency resulting in ketosis l acidosis and hyperglycaemia l
dehydration due to osmotic diuresis. Typically seen following missed insulin
treatments or infection in TDM, or as a first presentation ofTDM.
Diagnose based upon presence of hyperglycaemia (>mmol/ L), acidosis
(venous pH <7.3 or HCO
or ketonuria (≥2+). Stabilize the patient as described (E p. 338). Continue
−
<5mmol/ L), and blood ketones >3mmol/ L
3
fixed rate insulin infusion until ketones <0.6mmol/ L and pH >7.3. At
this point, convert to regular SC insulin if eating and drinking normally,
otherwise use a sliding scale; 2
<4mmol/L, start 0% glucose at 25ml/h alongside fluids.
Avoid hypoglycaemia once blood glucose is
All patients
with DKA should be reviewed by diabetic specialist nurses prior to discharge.
Hyperosmolar hyperglycaemic state (HHS)(E p. 339.)
K Severe, uncorrected hyperglycaemia leads to dehydration, but in the
presence of residual insulin production in T2DM, ketoacidosis does
not develop. Previously referred to as hyperosmolar non- ketotic state
(HONK). Diagnose based upon raised plasma osmolality (typically >320
mOsmol/ kg) with high glucose (typically >30mmol/ L).
Stabilize the patient as described in the treatment plan (E p. 339),then
continue IV fluid replacement based on clinical state and comorbidities (eg
elderly with heart failure) and seek cause. Patients with HHS should be reviewed by diabetic specialist nurses prior to discharge.
Prescribing insulinMany hospitals have separate drug cards for pre-
scribing insulin. Always specify the insulin formulation, and avoid using
the abbreviation ‘U’ for units (since this can be misread as a zero).
Variable rate intravenous insulin infusionAlso known as ‘sliding
scales’, these allow strict monitoring and control of blood glucose levels
for diabetic patients whose oral intake is significantly disrupted (eg NBM,
severe vomiting, or serious illness), and in critical illness, where good glycaemic control improves outcomes, eg post MI (Box .6). 3Variable
rate infusions are not suitable for patients with HHS or DKA.
Prescribe both the insulin infusion and appropriate IV maintenance uids on
the infusions section of the drug card. Prescribe insulin (eg. 50units actrapid
in 50mL 0.9% saline) to run alongside maintenance uids which
must con-
tain an appropriate glucose substrate (eg 0.45% NaCl with 5% glucose at
00mL/h). Follow local guidelines and give potassium in uids as required.
Stop a sliding scale once a patient is eating normally and able to resume
normal diabetes medication. Give normal dose of SC insulin 30min before stopping the scale, unless rapid acting (eg Novorapid
®
, Humalog®)
in which case give at same time as stopping thescale.
T Box .6 Adjusting variable rate insulin infusions
Persistent hyperglycaemia Check cannula and infusion pump. If no issues,
increase infusion rates by .5–2-fold and check ketones, venous pH, and
osmolality.
Hypoglycaemia Suspend infusion. Treat hypoglycaemia (E p. 337). Check
glucose is running concurrently. Once glucose >6mmol/L restart infusion at half the doses.
341HYPERGLYCAEMIA
342 CHAPTER Endocrinology
Diabetes mellitus
K Fasting plasma glucose ≥7.0mmol/ L, or ≥.mmol/ L 2h after a 75g
oral glucose load
tomatic or two occasions if no symptoms).
•
TDM Autoimmune pancreatic β- cell destruction, resulting in dependence
on exogenous insulin; typically presents in children or youngadults
•
T2DM Relative insulin hyposecretion or resistance to eects, requiring
drugs to potentiate insulin secretion or eects, or exogenous insulin;
typically occurs in adults, especially if overweight
•
Impaired glucose tolerance (IGT) HbA
plasma glucose ≥7.8mmol/ L after OGTT, but <.mmol/ L; 20–50%
progress to T2DM in 0yr
•
Impaired fasting glucose (IFG) Plasma glucose ≥6.mmol/ L after
an overnight fast, but <7.0mmol/ L; lower risk of developingT2DM
•
Gestational Any degree of glucose intolerance first detected during
pregnancy; around 50% will progress to T2DM within0yr.
TDM(E OHCMp. 200.)
SymptomsTiredness, weight loss, thirst, polyuria, abdo pain, vomiting.
SignsSweet- smelling breath, shock, abdominal pain (all suggestDKA).
InvestigationsGlucose testing as previously mentioned. Check venous HCO
and pH and ketones to exclude DKA. If uncertainty about type of diabetes,
positive islet cell or glutamic acid decarboxylase antibodies, or low C- peptide
levels all suggest TDM. Check HbA
TreatmentResuscitate and investigate for DKA; in the absence of DKA, a
new diagnosis of TDM does not necessitate admission, but the patient
should be started on a suitable insulin regimen by an appropriately experienced individual (eg endocrine registrar or diabetes nurse specialist)
with regular glucose monitoring and prompt out- patient follow- up. For
properties of some commonly used insulins E p. 202. Chronic management E p. 344. Involve diabetes teamASAP.
9
or HbAc >48mmol/ mol (on one occasion if symp-
42– 47mmol/ mol or
c
(Box.7).
c
−
3
K Box .7 HbA
c
HbAc reflects non- enzymatic glycosylation of haemoglobin at a rate proportional to plasma glucose. Since erythrocytes (and hence haemoglobin)
undergo slow but constant turnover, HbA
trol over the preceding – 3mth and is a reliable predictor of diabetes
complications. Target HbA
taking into account an individual’s risk profile, as well as tolerability of
levels should be set with patient involvement,
c
reflects plasma glucose con-
c
therapy. Initial targets in both TDM and T2DM are 48mmol/ mol with
looser targets applied if frail elderly or treatment refractory. In T2DM,
the target for patients on oral hypoglycaemic agents (eg. sulfonylureas) is
53mmol/L, with treatment intensification if levels rise to 58mmol/ mol.
9
In the presence of diabetes symptoms, a random plasma glucose ≥.mmol/ L may be considered
diagnostic; in the absence of symptoms, all tests should be repeated on a separate occasion.
0
Ie 86.5% (48mmol/ mol) and 87.5% (58mmol/ mol). Since 2009 HbAc levels have been re-
ported by NHS labs as mmol per mol (of haemoglobin without g lucose attached) but previous
units of % were reported in key trials, used in guidelines, and still permeate the consciousness of
some older patients and clinicians.
0