Добавил:
Sekretar
kiopkiopkiop18@yandex.ru
t.me/Prokururor I Вовсе не секретарь, но почту проверяю
Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз:
Предмет:
Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_3080_Библиотеки_им_академика_М_И_Перельмана
.pdf
The Patient with Respiratory Distress II
59
weakness can lead to reduced mobility and recurrent falls. Cognitive impair-
ment can be a signicant problem for many with PICS.
Post-
intensive care syndrome can predispose patients to many other psycho-
social issues including the following:
Personal relationships–disturbed sleep, sexual dysfunction, fatigue and
immobility can aect the patient’s relationships with those close to them.
Social isolation–immobility and depression may become a barrier for
usual social interactions.
Employment–patients may not be able to return to work in the same
capacity as previously.
See Case 11 for the ICU Liberation bundle (A–F) which has been proposed
as an approach to ICU management aiming to reduce the incidence of PICS.
Further reading
Leonhard, S., Mandarakas, M., Gondim, F. etal. (2019). Diagnosis and management
of Guillain–Barré syndrome in ten steps. Nat. Rev. Neurol. 15: 671–683. Evidence-
based guidelines for dealing with GBS.
Farrugia, M. and Goodfellow, J. (2020). A practical approach to managing patients
with myasthenia gravis– opinions and review of the literature. Front. Neurol. 11:
604. Overview of the medical management of myasthenia gravis.
Lee, M., Kang, J., and Jeong, Y. (2020). Risk factors for post- intensive care syndrome:
a systematic review and meta analysis. Aus. Crit. Care 33: 287–294. Systematic
review of risk factors for PICS.
https://t.me/medicina_free
Clinical Cases in Critical Care, First Edition. Alice Myers and Theophilus Samuels.
© 2023 John Wiley & Sons Ltd. Published 2023 by John Wiley & Sons Ltd.
4
Y
ou are called to urgently review a 46- year- old named Brian in the resus-
citation area of your emergency department (ED). He is a type 1 diabetic
patient complaining of severe abdominal pain but with no signs of peritonism.
His past medical history includes biliary colic. Observations reveal a systolic
BP between 85 and 95 mmHg, sinus tachycardia 130 bpm and an SpO
2
94% on
10 L/min oxygen. Brian has been vomiting profusely over the past 72 hours
and has not been taking his insulin during this time. His bedside serum blood
glucose is raised at 23
mmol/L and a spot urine test demonstrates the presence
of ketones.
The Patient with
Abdominal Pain
and Vomiting
What is the likely cause of this endocrine disturbance?
Brian is most likely in diabetic ketoacidosis (DKA).
Why do you suspect DKA?
Absolute insulin deciency–Brian has not been able to take his insulin
therapy. In type 1 diabetes mellitus (DM), there is a lack of circulating
endogenous insulin, which requires exogenous insulin for effective
management.
Relative insulin deciency–tissue insulin requirements are increased
by physiological stresses such as infection, trauma and major surgery.
Patients with type 1 DM can still develop DKA even if they take their
regular doses of insulin. Brian appears to be critically unwell, and so
probably has both an absolute and relative deciency.
Ketonuria –the presence of ketones in his urine is associated with DKA.
Describe the pathophysiology of DKA
Absolute or relative reduction in the eects of insulin –this leads to altered
carbohydrate metabolism. Patients with type 1 DM have virtually no
functional pancreatic beta- cells (where insulin is synthesised) and can
https://t.me/medicina_free
The Patient with Abdominal Pain and Vomiting
61
neither respond to changes in blood glucose levels nor maintain a basal
secretion of insulin. This absolute deciency aects metabolism in liver,
muscle and adipose tissue.
The increased hepatic production and decreased glucose uptake by
insulin-
dependent glucose transporter type 4 (GLUT4) receptors located
in muscle and adipose tissue result in hyperglycaemia.
Ketosis –this results from the rise in the counter- regulatory hormone
glucagon and other hormones such as cortisol, growth hormone and cat-
echolamines. This leads to the mobilisation of fatty acids from adipose
tissue, followed by increased hepatic beta-
oxidation and synthesis of
3-
hydroxybutyrate and acetoacetate. Also, in DKA, the clearance of these
ketone bodies is decreased, contributing further to the rise in ketone levels.
Renal threshold for handling glucose is greatly exceeded –the ensuing
hyperglycaemia leads to an osmotic diuresis resulting in loss of electro-
lytes and water. This results in dehydration, which in turn stimulates the
release of catecholamines, further exacerbating the problem.
Excess ketone bodies –result in a large amount of hydrogen ions needing
to be buered. This quickly depletes the buering capacity of the plasma,
allowing the ketone anions to accumulate, which leads to a raised anion
gap and contributes to the observed acidaemia.
How do you diagnose DKA?
Anion gap metabolic acidosis (bicarbonate <15 mmol/L and/or
venous pH <7.3).
Hyperglycaemia (commonly between 19.4 and 27.8 mmol/L) or known
diabetes mellitus.
Ketonaemia (>3 mmol/L) or signicant ketonuria (more than 2+ on a
standard urine dipstick test).
Glucose levels typically do not exceed 44 mmol/L. However, they may be
even higher in patients with DKA who are comatose.
How can the severity of DKA be classied?
Diabetic ketoacidosis can be classied as mild, moderate, or severe using var-
ious parameters including those listed here:
Mild–pH 7.25–7.30, serum beta- hydroxybutyrate 3–4 mmol/L
Moderate–pH 7.00–7.24, serum beta- hydroxybutyrate 4–8 mmol/L
Severe –pH <7.00, serum beta- hydroxybutyrate >8 mmol/L
Can a patient develop DKA with normal serum blood
glucose levels?
Yes. The class of drugs known as gliflozins (or sodium- glucose
co- transporter- 2inhibitors [SGLT- 2]) are a new group of oral medications used
in the treatment of type 2 diabetes. By inhibiting the SGLT- 2 receptors in the
renal tubules, they can prevent most glucose from being reabsorbed from the
https://t.me/medicina_free
Clinical Cases in Critical Care
62
glomerular ltrate to the plasma. This results in increased secretion of glucose
by the urine, improving blood glucose, as well as often promoting weight loss
and lowering blood pressure through the loss of sodium and water.
The DKA associated with these drugs is characterised by the usual meta-
bolic defects such as an anion gap metabolic acidosis, ketonaemia and reduced
plasma bicarbonate, but without the usual hyperglycaemia. This can occur
in type 1 patients when they are started on them to promote weight loss, for
example. Hence, in the absence of hyperglycaemia, the key for these individuals
is to test for either urinary or serum ketones when they feel unwell.
Explain why you consider this to be DKA and not a
hyperosmolar hyperglycaemic state (HHS)?
Essentially, HHS (also known as hyperosmotic hyperglycaemic non- ketotic state)
is a hyperglycaemic state without ketoacidosis that occurs most often in the
elderly and in those with known type 2 diabetes. It is commonly caused by acute
physiological stresses, such as infection, acute abdomen, cardiac or neurological
events. Drugs are also implicated, especially high-
dose thiazide diuretics, cortico-
steroids and beta- blockers. Typically, the blood sugar level is much greater (usually
33.3 mmol/L or greater) with a markedly elevated serum osmolality of 320 mOsm/
kg or greater. The mortality rates for HHS are higher than those for DKA.
The major dierence between these two conditions is that HHS patients
usually have enough circulating insulin to prevent ketoacidosis (prevents an
increase in free fatty acids and therefore blocks ketone production in the liver),
but not enough to prevent hepatic production of glucose and poor peripheral
utilisation by tissues. Some urinary ketones are still present and the anion gap
increases mildly, but the severe acidaemia seen in DKA is not observed. Hence,
the nausea and vomiting usually seen in DKA due to the severe acidaemia is
often absent. This potentially makes the onset of HHS very insidious as the
osmotic diuresis and hyperglycaemia can be quite protracted (days to weeks)
before medical attention is sought. This in turn can lead to severe electrolyte
abnormalities and severe dehydration, particularly in the elderly and frail.
So, given that Brian is a younger patient with type 1 diabetes and has had a
72-
hour history of nausea and vomiting with the presence of ketonuria, it is
more likely that he is in DKA than HHS.
How would you calculate and interpret the anion
gap for Brian?
The anion gap (AG) quanties the dierence between unmeasured cations
(positively charged ions) and unmeasured anions (negatively charged ions).
AG Na K Cl HCO
3
You are presented with the following blood results: Na
+
130 mmol/L, K
+
4.5 mmol/L, urea 8 mmol/L, creatinine 121 μmol/L and arterial blood gas analysis
(10 L/min oxygen therapy)–pH 7.21, PaO
2
44.1 kPa, PaCO
2
2.1 kPa, base excess
−9 mmol/L, bicarbonate 11 mmol/L, lactate 2.1 mmol/L, chloride 101 mmol/L.
https://t.me/medicina_free
The Patient with Abdominal Pain and Vomiting
63
The concentration of potassium is usually omitted, giving:
A
G Na Cl HCO
3
with the typical range equal to 4–12 mmol/L in the presence of a normal
albumin level (consult local laboratory reference ranges).
In healthy individuals, the anion gap mostly measures the negative charge
on albumin and phosphate, but it has a low sensitivity and low specicity and
is practically useless in the presence of hypoalbuminaemia.
What is the AG in this case?
The anion gap is raised at 130−(101 + 11)=18 mmol/L, so Brian has a high
anion gap metabolic acidosis due to severe DKA.
What are the causes for a raised AG?
Causes for a high anion gap can be outlined using the acronym GOLDMARK:
Glycols–such as ethylene and propylene. Propylene glycol is a common
diluent used for intravenous medications such as lorazepam. It is also
metabolised to L-
lactate and D- lactate.
Oxyproline (also called pyroglutaminic acid)–from chronic paracetamol
ingestion, especially in malnourished women.
L- lactate.
D- lactate (typically seen in patients with short gut syndromes).
Methanol.
Aspirin.
Renal failure.
Ketoacidosis (e.g. diabetes, starvation).
What are the main treatment goals when
managing DKA?
Commence insulin therapy and ensure that it is adequately reversing
the ketogenesis (e.g. by measuring capillary beta- hydroxybutyrate using
point- of- care testing).
Ensure acidaemia is improving and returning pH to the normal
physiological range.
IV uid therapy should adequately restore intravascular volume (typical
water decits are 100 mL/kg). Consult local guidelines on the rapidity of
uid resuscitation as these patients are prone to solute/water shifts that
leave them open to severe complications. The recommended resuscita-
tive uid is 0.9% saline.
Replace electrolyte losses, which can be severe (e.g. Na
+
, K
+
).
Treat the underlying cause(s).
Monitor for complications of DKA management.
https://t.me/medicina_free
Clinical Cases in Critical Care
64
How should insulin be prescribed to treat
patients in DKA?
The current recommendation is to start a fixed- rate intravenous insulin
infusion (FRIII) based on body weight and a serum glucose 14 mmol/L at
a rate of 0.1
units/kg/h. As soon as serum glucose decreases to <14 mmol/L,
a 10% dextrose infusion should be added. In addition, reducing the FRIII to
0.05
units/kg/h should be considered as this will reduce the risk of hypogly-
caemia and hypokalaemia developing (consult your local hospital guidelines).
What are the metabolic treatment targets in DKA?
Recommended targets are:
An increase in venous bicarbonate by 3.0 mmol/L/h
A reduction in blood ketone concentration by 0.5 mmol/L/h
A reduction in capillary blood glucose by 3.0 mmol/L/h
Maintaining serum potassium concentration between 4.0 and 5.5 mmol/L.
The FRIII rate should be increased if these targets are not met (also
consult your local hospital’s DKA protocol and/or a specialist in the
management of DKA).
What are the main complications from DKA that
would concern you?
Hyperkalaemia and hypokalaemia–these are potentially life- threatening
complications. Due to the pre- renal acute kidney injury that may occur
from severe dehydration, potassium replacement is not recommended
during the initial uid resuscitation or if the serum potassium level is
greater than or equal to 5.5 mmol/L. With insulin therapy, potassium
levels will almost always fall, so it is recommended that a ready- mixed
bag of 0.9% saline and 40
mmol/L of potassium are prescribed if the level
is less than 5.5 mmol/L and the patient is passing urine. If more concen-
trated solutions need to be given, this ideally should be done in a high-
dependency or critical care environment where the higher concentration
solutions can be given via a central vein with continuous monitoring.
Hypoglycaemia–blood glucose may drop sharply once insulin therapy
is commenced, and care should be taken to avoid dropping its levels to
less than the normal range. This can cause cardiac arrhythmias, acute
brain injury and death. In addition, it is imperative that rebound ketosis
is avoided as this will lengthen the duration of treatment. This occurs
when insulin falls to levels that create a relative deciency and allow the
counter- regulatory hormones to exert their ketogenic eects on metabo-
lism once again.
Cerebral oedema–symptomatic cerebral oedema is relatively uncommon
in adult patients with DKA. Cerebral oedema is known to occur within
the rst few hours of starting treatment, suggesting that it is iatrogenic
https://t.me/medicina_free
The Patient with Abdominal Pain and Vomiting
65
in origin. It is more commonly associated with children who pre-
sent with DKA.
Other –pulmonary oedema is a very uncommon complication and
usually occurs within the rst few hours of commencing treatment,
again suggesting an iatrogenic cause due to the rapid infusion of crystal-
loids over a short period of time. Those most at risk include the elderly
and those with impaired cardiac function. The development of venous
thromboembolic disease is also a potential complication, especially in
the presence of central venous catheters.
When would you consider this episode of DKA to
be resolved?
pH greater than 7.3
Bicarbonate level greater than 15.0 mmol/L
Blood ketone level less than 0.6 mmol/L
How long would you expect it to take for Brian’s DKA
to resolve?
Usually, by 24 hours of appropriate treatment, the ketonaemia and acidosis
should have resolved in most patients. However, should the patient fail to
respond to treatment, senior and specialist input should be sought. In addition,
other pathologies may be present that were dicult to identify during the
initial resuscitation period. Note, relying on serum bicarbonate concentration
only is not recommended. This is because a potential hyperchloraemic met-
abolic acidosis may be present due to the high volumes of 0.9% saline given.
With his previous history of biliary colic, what
do you think may be the cause of his severe
abdominal pain?
Gallstone disease is the most common cause of acute pancreatitis worldwide.
Brian’s history of biliary colic suggests the presence of gallstones. This would
need to be conrmed using either ultrasonography or CT.
Apart from acute pancreatitis, what other conditions
might cause his severe abdominal pain?
Diabetic ketoacidosis can often present with abdominal pain, but it should not
be ongoing if the patient is responding to treatment. Other causes could include:
Brian is transferred to your intensive care unit for monitoring and ongoing
management. After 24 hours, he is still severely acidotic. Brian is now
becoming increasingly confused and his abdominal pain is severe in the
epigastric area and radiates to his back. His most recent ABG on 10
L/min of
oxygen therapy demonstrates pH 7.01, base excess −17 mmol/L, bicarbonate
5 mmol/L and lactate 8 mmol/L.
https://t.me/medicina_free
Clinical Cases in Critical Care
66
Perforated viscus
Bowel obstruction
Ischaemic bowel
Myocardial infarction
Ruptured abdominal aortic aneurysm
Biliary colic, acute cholecystitis or cholangitis
Viral hepatitis and gastroenteritis
Sickle crisis
What are the causes of acute pancreatitis?
Gallstone disease or alcohol is the cause in 80% of cases in the developed world.
Alcohol-
induced pancreatitis should be considered when alcohol ingestion
greater than 50
g/day has occurred for at least 5 years. However, it is not always
possible to obtain such an accurate history. Apart from these two causes, the
others are rare and should only be considered if gallstone disease and alcohol
are not implicated. These causes and others can be remembered using the
mnemonic I GET SMASHED:
Idiopathic
Gallstones
Ethanol
Trauma
Steroids
Mumps/Malignancy
Autoimmune
Scorpion venom
Hyperlipidaemia, hypothermia, hypercalcaemia
Endoscopic retrograde cholangiopancreatography (ERCP)
Drugs (e.g. azathioprine, sulfonamides, OCP)
Which biochemical tests could you request
for presumed acute pancreatitis?
Serum amylase –due to its wide availability and sensitivity, this is
commonly requested. It may be normal in 10–20% of cases (especially
if the patient presents late in the course) and has low specicity.
Serum lipase–this increases within 4–8 hours and remains elevated
for 8–14 days and therefore is useful diagnostically in late presenta-
tions. It has a very high sensitivity for acute alcoholic pancreatitis. The
combination of both serum amylase and lipase will provide sensitivity
and specicity of 90–95% for detecting acute pancreatitis.
Serum triglyceride –this should be requested if a lipaemic serum is
suspected (e.g. triglyceride levels are above 11.3 mmol/L) or when the
cause of the pancreatitis is not clear.
Urinary trypsinogen- 2–this a novel test, which has a reported sensitivity
of 80% and specicity of 92%. It is not widely available.
https://t.me/medicina_free
The Patient with Abdominal Pain and Vomiting
67
Which imaging studies can be used in the diagnosis
of acute pancreatitis?
Ultrasonography (US)–an initial test that should ideally be performed
on all patients suspected of acute pancreatitis. It can be used in unstable
patients suspected of having gallstones or biliary disease. The use of
contrast- enhanced ultrasound has a reported sensitivity and specicity
of 82% and 89% respectively.
Endoscopic ultrasonography (EUS)–this is a combination of endos-
copy and ultrasound that is less invasive than ERCP and is useful in
diagnosing acute pancreatitis and choledocholithiasis. When CT and
US fail to show common bile duct stones, EUS may prove useful. Addi-
tionally, due to the absence of ionising radiation, it can be performed in
pregnant patients and those who are too unstable to be transferred out
of the critical care unit.
Computed tomography (CT)–the gold standard for grading acute pan-
creatitis and diagnosing pancreatic necrosis and peripancreatic collec-
tions. Although CT has a high accuracy, it does not usually need to be
performed before 72
hours unless the diagnosis is in doubt, or the patient
fails to improve clinically.
Endoscopic retrograde cholangiopancreatography (ERCP)–an effec-
tive means to treat common bile duct stones. It is, however, not indi-
cated in the treatment of mild pancreatitis or pancreatitis not due to
biliary disease.
Magnetic resonance cholangiopancreatography (MRCP) –with the
advantage of being non- invasive and not using ionising radiation, this
modality is able to depict abnormalities of the pancreatic duct and
parenchyma. Disadvantages of using MRCP include imaging artefacts
(e.g. gastrointestinal air or metallic clips) and increased acquisition time
compared to CT in a critically unwell patient at a remote site.
Which grading systems are you aware of for acute
pancreatitis?
Ranson’s criteria–with a reported sensitivity and specicity of 74% and
77% respectively, this scoring system uses 11 prognostic signs in total
at presentation and at 48 hours later. It was originally used for alcohol-
induced pancreatitis.
Glasgow–Imrie score–re- evaluating the Ranson’s criteria, it was found
that only eight of the 11 variables were predictive for mortality. This score
can be used for both biliary and non- biliary acute pancreatitis. Three or
more positive variables at 48 hours following admission suggest severe
pancreatitis and should prompt transfer to critical care (Table4.1).
You request an ultrasound of Brian's abdomen and pelvis, which demon-
strates a dilated common biliary duct. In conjunction with his signs and
symptoms and a grossly elevated serum amylase, you make the diagnosis
of acute pancreatitis secondary to gallstone- related disease.
https://t.me/medicina_free
Clinical Cases in Critical Care
68
APACHE II (Acute Physiology and Chronic Health Evaluation II)–used
throughout the world, this generic scoring system incorporates the
worst values within the rst 24
hours following admission to ICU and
is therefore not entirely suitable to monitor progress during the illness.
However, in predicting severe disease and hospital survival, it appears
to perform similarly when compared to the Ranson or Glasgow–
Imrie scores.
Atlanta classication–revised in 2012, this classication system grades
presentation clinically into the following categories:
Mild acute pancreatitis–no organ failure and no local or systemic
complications.
Moderately severe acute pancreatitis–organ failure that resolves
within 48 hours, local or systemic complications without persistent
organ failure.
Severe acute pancreatitis–persistent organ failure.
Balthazar index–this score assesses disease severity based upon CT
ndings. It should be noted that radiographic manifestations of acute
pancreatitis tend to lag behind the clinical condition.
Bedside index of severity in acute pancreatitis (BISAP) score–this can
be calculated relatively quickly at the bedside, and it uses the systemic
inammatory response syndrome (SIRS) criteria, along with age, urea
level, mental status and presence or absence of a pleural eusion to
predict mortality.
Why is grading the severity of acute pancreatitis
useful?
Potentially, by failing to recognise the more severe presentation of acute
pancreatitis, the lack of initial aggressive management and support may lead
to increased morbidity and prevent the appropriate resources being allocated.
Furthermore, it is important that a patient with severe acute pancreatitis is
managed in an intensive care unit.
Table 4.1: Glasgow–Imrie score for acute pancreatitis. The variables can be
remembered using the mnemonic PANCREAS.
PaO
2
<8 kPa
Age >55
years
Neutrophils WBC
>15 × 10
9
/L
Calcium <2
mmol/L
Renal function Urea >16
mmol/L
Enzymes LDH
>600 IU/L, AST >200 IU/L
Albumin <32
g/L (serum)
Sugar Blood glucose >10
mmol/L
AST, aspartate aminotransferase; LDH, lactate dehydrogenase.
https://t.me/medicina_free
Соседние файлы в папке Библиотека им академика М.И. Перельмана