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12 Surgical Intensive Care
Hyponatremia
Symptoms Headache, Nausea, vomiting, seizures
Severe hyponatremia (<120mEq/L) may lead to lethargy, headaches, seizures, and coma
403
Sodium decit
calculation
Management
Sodium decit=(140-Na+)×TBW
Rapid correction of sodium may lead to central pontine myelinolysis
➔acute correction: 6–12mEq/L in 24h
➔chronic correction: Less than 8mEq/L in 24h
Hypovolemic Euvolemic Hypervolemic
• Diuretic abuse
(elevated urine Na+)
• Emesis/diarrhea
Causes
Normal saline • Fluid restriction
Management
• SIADH: Increased
ADH (low serum
osmolality; elevated
urine Na+ and
osmolality)
• Psychogenic
polydipsia (low
serum osmolarity;
urine N+ + and
osmolarity low)
• Adrenal insufciency
• Exercise-induced
hyponatremia
• Hypothyroidism
• Hyperglycemia
induced
hyponatremia
• Hypertonic saline
• Vasopressin
antagonist (tolvaptan,
conivaptan)
• Cirrhosis
• Congestive heart
failure
• Nephrotic
syndrome
• Renal failure
Furosemide with
hypertonic saline
SIADH Can be due to traumatic brain injury/ lung malignancy/lung infection/pain
Increased ADH ➔ decrease urine output, hyponatremia, decreased serum osmolarity, urine
osmolarity >150mmol/kg, urine Na+>25mmol/L
➔Absence of Hypokslemia differentiate SIADH and adrenal insufciency
Management: acute ➔ tolvaptan
Chronic ➔ uid restriction and diuresis
404
+
–w
T wave
Данная книга находится в списке для перевода на русский язык сайта https://meduniver.com/
Hypernatremia
Symptoms Irritability, restlessness, seizure
Hypovolemic Euvolemic Hypervolemic
A. H. Sohail et al.
Management
Diabetes insipidus
Free water decit
calculation
• Osmotic diuretic
use
• Post-obstructive
Causes
Management
Rapid correction of sodium may lead to cerebral edema
➔acute and chronic correction: less than 8mEq/L in 24h
Central diabetes insipidus results from head trauma, lithium, and neurosurgery
Decreased release of ADH from hypothalamus
Increased urine output, hypernatremia, increased serum osmolarity
Management: Acute ➔ DDAVP; chronic ➔ free water
Equation for free water deficit
diuresis
• Intrinsic renal
disease
• Burns
• Diarrhea/stula
• Normal saline to
restore volume
Then hypotonic
saline solution
Na
140
• Diabetes insipidus
Central
Nephrogenic
• Hypodipsia
• Insensible uid
losses
• Free water
replacement
1
Total body =
×
• Hyperaldosteronism
Primary
Secondary
• Cushing syndrome
• Exogenous/iatrogenic
(treatment with
hypertonic solutions
• Free water replacement
weight
Hypokalemia
Causes
Presentation Ileus, weakness, and cardiac arrhythmias
EKG changes
Management Replace potassium and magnesium
High-volume emesis, diarrhea, stulas, diuresis, or inadequate intake
Potassium is driven intracellularly and into the urine during alkalotic states
T wave disappears
Depressed ST
U wave formation
Prolonged QT
ST depression
Shallow
U wave
Widened QRS
T wave
12 Surgical Intensive Care
Hyperkalemia
Causes Renal failure, rhabdomyolysis, tumor lysis syndrome, transfusion, medications
Presentation Muscles weakness, tiredness, and fatigue
405
EKG changes Peaked T waves
Wide QRS complexes
ST depression
Management Prevent potassium induced effects with the administration of calcium
Give NS and diuretics (Lasix)
High-dose nebulized albuterol
Glucose and insulin administration
Treat acidosis (bicarbonate)
Potassium binders: Kayexalate/Lokelma
Dialysis
Hypocalcemia
Causes Pancreatitis, tumor lysis syndrome, or hypoparathyroidism
Presentation Perioral tingling and numbness, hyperreexia
A positive Chvostek sign (muscle spasm after tapping on the facial nerve)
A positive trousseau sign (muscle spasm of the extremity after squeezing of blood
pressure cuff)
Peaked
EKG changes Prolonged QT interval
T-wave inversion
Heart block
Management
Calculate corrected calcium=0.8×(Normal albumin−Serum albumin)
Replete magnesium before repleting calcium
406
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Hypercalcemia
Causes Hyperparathyroidism: Most common cause (especially in outpatients)
Malignancy: Breast cancer (especially in hospitalized patients)
Sarcoidosis
Presentation Lethargic state, nausea, vomiting, hypotension
Shortened QT interval
EKG changes
T-wave widening
Atrioventricular block
A. H. Sohail et al.
Management
Acute ➔ Normal saline then diuresis
For malignant disease➔bisphosphonates
Hypomagnesemia
Causes Diuresis, alcohol abuse
Presentation Hypomagnesemia is serious and potentially deadly electrolyte abnormality.
Leads to hypokalemia
Confusion, irritability, hyperreexia, and seizure
EKG changes Widened QRS
Transition from peaked T waves to attened T waves
Prolonged PR interval
Polymorphic ventricular tachycardia
Management Replete magnesium
Hypermagnesemia
Causes Renal failure and medications that contain magnesium (laxatives, antiacids)
Presentation Hyporeexia, lethargy, muscle weakness, hypotension, nausea, and emesis
EKG changes Peaked T-waves
Bradycardia
Management Calcium
Hyperphosphatemia
Causes Associated with renal failure
Rhabdomyolysis, tumor lysis syndrome, hemolysis, and malignant hyperthermia
Presentation Largely asymptomatic
Management Phosphate binders, low phosphate diet, might require dialysis
12 Surgical Intensive Care
Hypophosphatemia
407
Causes Secondary to an intracellular shift of phosphorus in association with respiratory alkalosis,
insulin therapy, refeeding syndrome, and hungry bone syndrome
Presentation
Cardiac dysfunction and muscle weakness ➔ failure to wean from ventilator
Management Phosphate repletion
Acid-base disorders
The body’s pH level is maintained by the lungs and the kidneys
Acid-base disorders are compensated by changes in ventilation and excretion of bicarbonate and
Characteristics
Metabolic
acidosis
acids
Ventilation causes an acute response to acid-base derangements
Renal compensation takes hours to days
Acid accumulation or loss of bicarbonate
Respiratory compensation for a metabolic acidosis: pCO2=1.5×[HCO
Anion gap=Na– (HCO
-
+Cl-)
3
–
3
]+8
Normal anion gap=8–16mEq/L
High anion gap=methanol, uremia, diabetic ketoacidosis, paraldehyde, Isoniazide, lactic
acidosis, ethylene glycol, salicylates, strychnine (MUDPILES)
Metabolic
alkalosis
Normal anion gap acidosis=high- volume lower GI losses, renal tubular acidosis
Usually, a contraction alkalosis due to loss of acids or increased serum bicarbonate
Often associated with hypokalemia secondary to intracellular drive to exchange hydrogen ions
Nasogastric suction/high-volume emesis ➔ hypochloremic, hypokalemic metabolic alkalosis
with paradoxical aciduria
• Loss of H+ and Cl- from stomach
• Hypovolemia ➔ kidney reabsorb Na+ in exchange of K+ ➔ hypokalemia
Na+/H+ exchanger activated to reabsorb water and K+ ➔ paradoxical aciduria
Management: NS to correct Cl- decit
408
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Acid-base disorders
A. H. Sohail et al.
Respiratory
acidosis
Respiratory
alkalosis
Increased concentration of carbon dioxide is due to inadequate alveolar ventilation
Equations
• Acute compensation Δ pH=(pCO2– 40)×0.08
• Chronic compensation Δ pH=(pCO2– 40)×0.03
Treatment of acute respiratory acidosis is directed at the underlying cause
Short-term management involves measures that increase minute ventilation: Increased respiratory
rate and tidal volumes
Pregnancy, high altitude, pain, anxiety, and medications (progesterone) are common causes ➔
this involves decreased concentration of carbon dioxide due to hyperventilation
Renal Disturbances
Renal disturbance
Prerenal causes Due to decreased renal perfusion
Causes of AKI
Intrinsic renal causes Renal parenchymal disease (Acute tubular
Postrenal causes Obstruction of urine outow
(hypovolemia)
necrosis, tubulointerstial nephritis)
Glomerular ltration
rate(GFR)
Fractional excretion of
sodium (FENa)
Fractional excretion of
urea (FEurea)
GFR measures the working capacity of the kidney
GFR≈creatinine (Cr) clearance=(UCr/PCr)×V (volume of urine/minute)
FENa=(urine Na×serum Cr)/(serum Na x urine Cr)
FE
(urine urea x serum Cr)/(serum urea × urine Cr)
Urea=
12 Surgical Intensive Care
Renal disturbance
409
Diagnosis
Radiography
Management
Urinalysis
Prerenal Intrinsic renal Postrenal
Urine osmolality
(mOsm/kg)
Urine sodium
(mEq/L)
FENa (%) <1% >2% >4%
FEUrea (%) <35% 50–65%
BUN/Cr >20 <15 > 15
• Renal ultrasound ➔to rule out obstructive uropathy
• Kidney-ureter-bladder (KUB)➔ identies radiopaque stones
Fluid balance
• If hypovolemia ➔replaces losses with isotonic uid
If euvolemia or hypervolemia ➔uid restriction
Assess acid-base status and maintain pH >7.15
>500 <350 <350
<10 >20 >40
+RBCs➔ intrinsic or obstructive
+WBCs➔urinary tract infection
+nitrates or leukocyte esterase➔urinary tract
infection
+Esoinophils➔allergy or drugs
Casts➔intrinsic kidney disease
Proteinuria➔intrinsic kidney disease
Correct electrolytes
Discontinue nephrotoxic drugs and adjust doses of renally excreted drugs
• Acidosis
Indications for renal
replacement
Modalities of renal
replacement
Outcomes Patients requiring renal replacement therapy for AKI have a 50% mortality rate
• Electrolyte abnormalities
• Intoxicants
• Fluid Overload
• Symptomatic Uremia (severe altered mental status, uremic pericarditis, bleeding)
Intermittent hemodialysis Flow rate>300ml/min
Requires stula, graft or double lumen CVC
Continuous renal replacement therapy
(CRRT) or continuous veno-venous
hemoltration (CVVH)
Flow rate>200ml/min
Requires double lumen CVC
➔used for hemodynamically unstable
patients
410
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Research
A. H. Sohail et al.
Reference Findings
Su X, Xie X, Liu L, Lv J, Song F, Perkovic V, Zhang
H.Comparative effectiveness of 12 treatment strategies
for preventing contrast-induced acute kidney injury: a
systematic review and bayesian network meta-analysis.
Am J Kidney Dis. 2017;69(1):69–77
Ricci Z, Cruz D, Ronco C.The RIFLE criteria and
mortality in acute kidney injury: a systematic review.
Kidney Int. 2008;73:538–546
Neurological Disturbances
Alcohol withdrawal
Presentation
Alcohol withdrawal may include seizures, alcoholic hallucinosis, delirium tremens, severe
hypertension, uid and electrolyte disorders, tachyarrhythmias, and death
Management of severe alcohol withdrawal focuses on the management of psychomotor
agitation with benzodiazepines
Patients are monitored with a CIWA-AR (clinical institute withdrawal assessment alcohol
revised) score
When CIWA-AR score ≥8 ➔ medication is given
Medication Indication Dose
Current guidelines recommend intravenous volume
expansion with isotonic crystalloid solution before
and after intravascular contrast use as the cornerstone
treatment for the prevention of contrast- induced AKI
This systematic review of 24 studies showed a
stepwise increase in relative risk for death with
increasing AKI severity (risk, 2.40; injury, 4.15;
failure, 6.37, with respect to non-AKI patients)
Management
Benzodiazepines 1st line therapy
Give if patient refractory
Barbiturates
Propofol
Centrally acting α-2 against
(dexmedetomidine
(Precedex), clonidine)
to high-dose
benzodiazepine
If patient refractory to
benzodiazepine and
barbiturates
Should not be used as
primary treatment
Diazepam (5–10mg) IV
Lorazepam (2–4mg) IV if
severe liver disease
Or
Chlordiazepoxide (25–
100mg) PO Oxazepam
(10–30mg) PO if severe liver
disease
Phenobarbital 130–260mg
IV
1mg/kg
12 Surgical Intensive Care
Delirium
Pathophysiology
411
Stress inammation, neuronal injury, melatonin deciency, and abnormal levels of
neurotransmitters might lead to delirium
One theory is that delirium is secondary to deciency in the cholinergic system
(acetylcholine)
Age and underlying cognitive impairment ➔ most common preexisting conditions
Risk factors
Presentation
Diagnosis
Types
Age greater than 70years, existing cognitive or functional impairment, vision
impairment, history of alcohol abuse, abnormal electrolytes, poor functional status,
and type of surgery
Delirium is the most common postoperative complication in elderly
Changes in the sleep-wake cycle, hallucinations or delusions, mood changes, and
autonomic dysregulation
Postoperative delirium normally develops 24–72h postoperatively
A disturbance in attention and awareness over a short period (usually hours to days)
that tends to uctuate during the course of the day
A change in cognition
Absence of another explanatory disorder
Type Description Prognosis
Hyperactive delirium Patients are restless and/
or agitated
Hypoactive delirium Patients are lethargic and/
or apathetic
Mixed delirium Patients have periods of
both hyperactivity and
hypoactivity
Associated with higher
mortality and often
underdiagnosed
Emergence delirium Inappropriate motor
behavior, disorientation,
and emotional lability
It most commonly
presents at postanesthesia care unit
admission
Resolves in a few hours
It does not have a
uctuating course
412
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Delirium
A. H. Sohail et al.
Diagnosis Onset Description
Consciousness reduced
Differential diagnosis
Confusion assessment
method (CAM) score
Delirium Acute onset
Dementia Insidious onset
Depression Insidious or acute
CAM score ➔most widely used screening test used to check for the presence of
delirium
The diagnosis of delirium by CAM requires the presence of features 1 and 2 and
either 3 or 4
1: Acute onset or uctuating course
2: Inattention
3: Disorganized thinking
4: Altered level of consciousness
Attention is impaired
Hallucinations are very
common
Consciousness and
attention remain
unimpaired until late stages
Hallucinations are
uncommon
Consciousness is clear
Attention may be
disorganized
Hallucinations are
uncommon
Postoperative delirium is preventable in up to 40% of cases
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