Workup may include imaging (abdominal x-ray, CT scan), CBC, CMP, lactate level
Trial of conservative (nonsurgical) management appropriate if no evidence of perforation, ischemia, or strangulation
Bowel rest and decompression with nasogastric (NG) tube are appropriate first steps
Start GI prophylaxis with Ranitidine (Zantac) 50 mg IV every 8 hours or proton pump inhibitor [eg, pantoprazole (Protonix)]
Replace NG tube output [1 cc NS (or LR) per cc NG tube output every 4 hours] and replete electrolyte losses
Note: If obstruction occurs acutely within 1 week of surgery, high likelihood of requiring surgical intervention
If conservative management fails
Consider risks/benefits of surgical intervention: Consent for exploratory laparotomy, possible bowel resection, possible bypass, possible ostomy
Consider preoperative Gastrografin enema to rule out concurrent large bowel obstruction (LBO)
Surgery not appropriate in patients with poor prognostic criteria (ie, diffuse intra-abdominal carcinomatosis, multifocal obstruction, poor performance status, or massive ascites)
Note: For women with ovarian cancer and bowel obstruction, data show 90% relieved with surgery, but major morbidity (fistulas and anastomotic leaks) occurred in 32% and perioperative death in 15%. Re-obstruction rate of 10–50%
If the patient is not a surgical candidate, consider percutaneous endoscopic gastrostomy (PEG) tube
Octreotide (100-300 μg subcutaneously 2-3 times daily) can decrease gastric secretions and slow intestinal mobility → decreases nausea/vomiting associated with SBO
Obstruction at cancer diagnosis and mucin histology are associated with recurrent obstructions
Rare in ovarian cancer patients
In general, considered a surgical emergency
Surgical management generally involves creation of an ostomy
Endoscopic management with rectal stent is possible in select patients (stable, no peritoneal signs, partially obstructed, poor surgical candidate)
In general, considered a surgical emergency
Commonly due to adhesions. Occurs when two points along the small bowel are obstructed at the same junction, causing necrosis and edema of the internal segment
May look like a gasless abdomen on plain films. CT usually diagnostic and may show ground glass haziness in mid-abdomen, displacement of adjacent bowel, dilated clumps of edematous bowel, or classic U or C signs (pathognomonic)
Bisacodyl (Dulcolax) 10 mg orally daily or 10 mg per rectum daily
Docusate sodium (Colace) 100 mg orally twice daily
Mineral oil 15–45 mL/day
Cascara 325 mg orally nightly
Polyethylene glycol (MiraLax) 240–720 mL/day
Lactulose 15–30 mL twice daily
Sorbitol 120 mL of 25% solution daily
Glycerin 3 g per rectum daily or 5–15 mL enemas
Remember: All patients on around-the-clock opiates should be on a bowel regimen
Consider in patients with high-output ileostomies or short bowel syndrome in order to avoid dehydration and other electrolyte abnormalities, including hypocalcemia, hypomagnesemia, or hypokalemia
Be mindful of stoma outputs greater than 1000 cc/day
Loperamide (Imodium) 2 mg orally three times daily
Diphenoxylate/atropine (Lomotil)—requires narcotic prescription—2.5 mg orally three times daily
Tincture of opium 6 mg orally four times daily—sometimes in drop form (2 drops three times daily may be sufficient)—requires narcotic prescription
Note: Patient education on self-management is crucial
Transcellular shift: Metabolic alkalosis, insulin, β agonists
Extrarenal: Decreased K intake, GI losses including vomiting and diarrhea
Renal: Diuresis, hyperaldosterone (primary, secondary), increased glucocorticoids (Cushing’s syndrome), renal tubule disease (renal tubular acidosis)
Diffuse muscle weakness; change in mental status
ECG changes: Earliest change is flattened T waves, followed by inversion, U waves may be visible, ST-segment depression, arrhythmias
Check magnesium as hypomagnesemia can cause refractory hypokalemia. Magnesium level must be corrected for potassium repletion to be effective
<3 mEq/L: 40 mEq KCl IV minibag over 4 hours (administer twice)
3.0–3.5 mEq/L: 40 mEq KCl IV minibag over 4 hours once, or 40 mEq potassium chloride (KDur) orally every 4 hours
<2.5 mEq/L: Obtain ECG and replace as above
Do not replace faster than10 mEq/h.
Serum K rises approximately 0.1 for every 10 mEq given
Transcellular shift: Metabolic acidosis, insulin deficiency, β blockers, tissue damage
Extrarenal: Excessive potassium intake
Renal: Hypoaldosteronism, acute or chronic renal failure
Other: Decreased volume, K-sparing diuretics
Pseudo-hyperkalemia may be caused by blood draw secondary to hemolysis
ECG changes: Increased T wave amplitude, prolonged PR interval, increased QRS duration, loss of P waves, sine wave pattern, ventricular fibrillation, asystole (Figure 3-1)
Calcium gluconate 1 g over 2-3 minutes (decreases membrane excitability)
Insulin/Glucose (shifts into cells)
Ex: Insulin 10 units followed by 1 amp D50, then D5-NS at 50 cc/h for 6 hours
OR 4 units insulin after 1 L bolus D5
Kayexalate (binds potassium)
Dialysis
Ca <8.4 mg/dL. Calcium gluconate 1 gram over 2 hours, or CaC03 650 mg orally three times daily
Need to correct Ca for serum albumin: for every 1.0 decrease in albumin less than 4.0, add 0.8 to Ca to replace for corrected calcium <8.4 mg/dL
Primary hyperparathyroidism, malignancy, thyrotoxicosis, chronic kidney disease, milk alkali syndrome, hypervitaminosis D, sarcoidosis, lithium, thiazide diuretics, pheochromocytoma, adrenal insufficiency, rhabdomyolysis/acute renal failure, theophylline toxicity, familial hypocalciuric hypercalcemia, metaphyseal chondrodysplasia, congenital lactase deficiency
In cancer, hypercalcemia is often associated with advanced disease and poor outcomes
Labs
Serum parathyroid hormone (PTH) (if elevated, primary hyperparathyroidism is diagnosis). There is an increased frequency of primary hyperparathyroidism in the oncology population, so this is reasonable to evaluate
If serum PTH is low/normal, send PTH-related protein and vitamin D metabolites (calcidiol and calcitriol) to evaluate for hypercalcemia of malignancy and vitamin D intoxication.
Consider bone scan if you suspect malignancy
Additional labs that may be useful if picture still unclear: Serum and urinary protein electrophoresis (for possible multiple myeloma), TSH, vitamin A, serum phosphate, urinary 24 hour calcium
Patients who are symptomatic, have an acute rise, or who have a calcium concentration over 14 mg/dL (3.5 mmol/L) require treatment
Isotonic saline at 200–300 cc/h (corrects hypovolemia and urinary salt wasting), tapered down to urine output of 100–150 mL/h. Monitor carefully especially in patients with edema/heart/kidney problems. If edema develops, stop IV fluids and consider loop diuretic
Calcitonin 5 IU/kg IM every 12 hours, but can increase to 6–8 IU/kg every 6 hours. Tachyphylaxis develops in 48 hours. Nasal calcitonin is not efficacious
Bisphosphonates (maximal effect occurs in 2–4 days)
Replacement (keep Mg above 1.7 mEq/L)
<1 mEq/L: MgSO4 6 g IV minibag over 6 hours
1.1–1.3 mEq/L: MgSO4 4 g IV minibag over 4 hours
1.4–1.6 mEq/L: MgSO4 2 g IV minibag over 2 hours
Oral: Magnesium oxide 400 mg orally three times daily
Replacement
Phos <2.7 mg/dL: K-phos or Na-phos 15–20 mmol IV minibag over 6 hours. If taking orally, Neutra-Phos 250 mg orally three times daily
Neutra-Phos contains approximately 8 mmol Phos/250 mg and 7 mEq K/250 mg
Hyperphosphatemia may be seen in patients with chronic kidney disease. These patients should typically be on calcium acetate (PhosLo)
Calculate serum osmolality: 2 × Na + glucose/18 + BUN/2.8
Osm >295 (Hypertonic): Hyperglycemia or mannitol treatment
Osm 280–295 (Normal): Increased lipids
Osm <280 (Hypotonic): Evaluate volume status, check urine Na
Prevent central pontine myelinolysis—don’t correct too quickly
Syndrome of Inappropriate Antidiuretic Hormone Secretion (SIADH): A condition when excess ADH is excreted, typically resulting in decreased urine output, hyponatremia
Treatment: Find the underlying cause that can be due to CNS disturbances of malignancy (especially lung). Treat the underlying cause and correct the sodium slowly with normal saline
ELECTROLYTE ABNORMALITIES: QUICK MANAGEMENT GUIDE
Cause | EKG Changes | Management |
---|---|---|
Hypokalemia (<3.5 mEq/L) | ||
Transcellular shift Diuretics Renal loss NG tube Magnesium depletion Diarrhea Insulin | T wave inversion/ flattening U waves ST depression | Replete Mg and K |
Hyperkalemia (>5.5 mEq/L) | ||
Transcellular shift Acidosis Beta blockers Digoxin NSAIDs Heparin ACE inhibitors Succinylcholine Transfusion Renal insufficiency Adrenal insufficiency Potassium-sparing diuretics | Peaked T waves Flattened P waves More severe
| Membrane antagonism
Transcellular shift
Enhanced clearance
|
Hypocalcemia (< 8.4 mg/dL) | ||
Magnesium depletion Sepsis Alkalosis Blood transfusion Aminoglycosides Heparin Renal failure Pancreatitis Hypoparathyroidism Tumor lysis syndrome | Prolonged QT Ventricular tachycardia | Replete calcium |
Hypercalcemia (>12 mg/dL) | ||
Hyperparathyroidism Malignancy | Shortened QT interval | Administer NS Lasix Hydrocortisone Bisphosphonate Calcitonin Mithramycin (Plicamycin) Dialysis DO NOT GIVE D5W |
Hyponatremia (<135 mEq/L) | ||
Hypovolemic
Normovolemic
Hypervolemic
| Hypovolemic
Normovolemic
Hypervolemic
| |
Hypernatremia (>145 mEq/L) | ||
Hypovolemic
Normovolemic: (ADH defect)
Hypervolemic: Salt, NaHCO3 infusion | Hypovolemic: Slow fluids with NS/albumin, then free water Normovolemic: Free water Hypervolemic: Lasix versus observation Rapid correction → cerebral edema | |
Hypomagnesemia | ||
Lasix Aminoglycosides Cisplatin Alcohol Diabetes Acute myocardial infarction Diarrhea | Torsades de pointes Prolonged QT | Magnesium repletion |
Hypermagnesemia | ||
Renal insufficiency Hemolysis Diabetic ketoacidosis Adrenal insufficiency Hyperparathyroidism Lithium intoxication | Dialysis Calcium gluconate NS/Lasix | |
Hypophosphatemia | ||
Glucose loading Sepsis Respiratory alkalosis Diabetic ketoacidosis Beta receptor agonists | Phosphate repletion (Na-Phos or K-Phos) Very important in liver resection | |
Hyperphosphatemia | ||
Associated with hypocalcemia |
CT Scan: Sensitive to tumors approximately 1–2 cm
PET Scan: Sensitive to approximately 8 mm
Contrast Dye Allergy
Pre-treat with Prednisone 40 mg orally 24 hours before scan, 12 hours before, and immediately before scan
Elevated Creatinine: Be particularly careful in patients with glomerular filtration rate (GFR) < 60mL/min or creatinine 1.5 or above (especially if diabetic). If there are no contraindications to volume expansion, pre-treat with IV isotonic bicarbonate (6 mL/kg) 1 hour prior to the procedure and 1 mL/kg/h for 6–12 hours following the procedure (longer for patients with severe renal impairment). If isotonic saline (1 mL/kg/h) is used, this can also be administered 6 hours prior to and 6 hours after the procedure
Clinical suspicion: Dyspnea, tachycardia, hypoxia, sense of impending doom
Workup
Arterial Blood Gas (ABG)—look for A-a gradient [A-a grad = 148 – 1.2 (Paco2) – Pao2]
Equation presumes patient is breathing room air at sea level (Fio2 = 0.21)
A-a gradient is influenced by age and inspired oxygen. A normal gradient rises with age. Can be as high as 25–35 mm Hg for patients over age 40
For patients on supplemental O2, the normal A-a gradient increases 5–7 mm Hg for every 10% increase in Fio2
ECG if tachycardic
Chest x-ray to look for another cause of desaturation
Spiral CT of chest
Lower extremity Dopplers to evaluate for DVT
Wells Criteria: Determine likelihood of PE (>4 points—very likely)
| 3 points |
| 3 points |
| 1.5 points |
| 1.5 points |
| 1.5 points |
| 1 point |
| 1 point |
Treatment
LMWH or UFH drip are equivalent treatment; then transition to warfarin (Coumadin) if appropriate (start 5 mg orally daily for 2 days, then adjust according to INR)
LMWH: Enoxaparin (Lovenox) 1 mg/kg SQ every 12 hours
LMWH doesn’t require monitoring or dose adjustment but has longer half-life (which makes it more difficult to have lines placed, epidurals pulled, etc)
UFH
BE CAREFUL BEFORE STARTING HEPARIN BOLUS ON POST-OP PATIENT DUE TO BLEEDING RISK!! CONSIDER STARTING MAINTENANCE DOSE ONLY
To Start UFH Treatment
Baseline labs: aPTT/PT/INR, CBC, basic metabolic panel
Monitor CBC daily until UFH is discontinued
If CBC is normal for 7 consecutive days, can decrease frequency of obtaining lab to not less than every 3 days up to day 14. If stable at that point, can obtain weekly
See Table 3-3 for UFH Nomogram
Anti-Xa UFH activity
Measures anticoagulant activity of UFH directed against factor Xa
Not affected by lupus anticoagulant, factor VIII or XII activity, warfarin levels
No lot-to-lot variations
Studies have shown that patients monitored with Anti-Xa UFH activity can achieve therapeutic levels more quickly and require fewer monitoring tests compared to patients monitored with aPTT
Therapeutic range remains constant (0.3–0.7 IU/mL)
Drawn every 6 hours after initiation of therapy (or dose change) until two therapeutic levels are obtained, then daily
CAREFUL: There are Anti-Xa LMWH tests (for monitoring LMWH) and Anti-Xa UFH tests (for monitoring UFH)
Transitioning
Transition from UFH to LMWH
Discontinue UFH concurrently with first dose of LMWH
UFH or LMWH to Warfarin Transition
During treatment of acute thrombosis, UFH (or LMWH) is continued for at least 5 days and the INR needs to be in goal range for at least 24 hours before UFH (or LMWH) is discontinued
Remember: Warfarin dose is not reflected in INR for 2–3 days post dose change; daily increases in dose are not recommended
Choice of long-term anticoagulant
Warfarin relies on a steady intake of vitamin K, and cancer patients have wide fluctuations in their dietary habits for a variety of reasons (chemotherapy, bowel obstructions, etc). Some data suggest that cancer patients have improved outcomes with LMWH compared to warfarin. However, LMWH is very expensive
See Table 3-4 for trials on anticoagulation
UFH NOMOGRAM
Heparin Nomograms | aPTT Goal |
---|---|
Standard: Atrial fibrillation, VTE, arterial thromboembolism, mechanical valve, obstetric VTE prophylaxis, peripheral vascular disease | 50–80 seconds |
Low: Age over 70, pulmonary hypertension, ischemic stroke in patient with atrial fibrillation, patient with acute coronary syndrome (including those on GP IIB/IIIA inhibitors or fibrinolytics) | 50–65 seconds |
High: Vascular surgery patients | 65–80 seconds |
Postsurgical: Ventricular assist device patients, organ transplant patients (main difference between this nomogram and low goal is the lack of bolus) | 50–65 seconds |
ANTICOAGULATION TRIALS
Trials | Conclusions |
---|---|
CLOT trial | RCT—dalteparin associated with half the risk of recurrent VTE in cancer patients compared to warfarin |
CANTHANOX trial | RCT—warfarin associated with a statistically significant increased risk of bleeding and twice the risk of recurrent VTE (but this was not statistically significant) when compared with Lovenox. |
Cochrane review | LMWH compared to vitamin K antagonists (ie, warfarin)—LMWH associated with less recurrent VTE, but no change in overall survival or bleeding |
Packed Red Blood Cells (PRBCs): Most plasma has been removed; total volume of 1 unit of PRBCs is about 250–300 cc; hematocrit should increase by 3% or hemoglobin by 1 g/dL
Platelets: 1 “pack” (6 units) should raise the count by 5000–8000.
When to transfuse platelets
Part of resuscitation with PRBCs
Platelets less than 10 000 (to prevent spontaneous hemorrhage)
Platelets less than 50 000 if about to undergo procedure, are actively bleeding, or have a qualitative platelet disorder
Platelets less than 100 000 (in patients with CNS injury, multisystem trauma, undergoing neurosurgery, or who require an intrathecal catheter)
Normal platelet count but ongoing bleeding and a reason for platelet dysfunction (congenital disorder, chronic aspirin therapy, uremia)
Cryoprecipitate: Contains Factor VIII, Factor XIII, von Willebrand’s Factor, and fibrinogen. One unit is about 10 cc
Fresh Frozen Plasma (FFP): Contains clotting factors. FFP must be thawed in a 37 degree C waterbath. This usually takes about 30 minutes. FFP has only a 24-hour shelf life; therefore, it is best ordered the same day it will be used. One unit is about 150–250 cc
When transfusing PRBCs
Premedicate with (prior to each unit)
Tylenol 650 mg orally/rectally once
Diphenhydramine (Benadryl) 25 mg orally/IV once
Each unit should be run in over 3–4 hours
Premedication does not necessarily decrease febrile non-hemolytic transfusion reactions
Patients with cardiac risk factors may need furosemide (Lasix) (10–20 mg) in between units to prevent volume overload (avoid Lasix in the sulfa-allergic patients)
When replacing large volumes of PRBCs, replace platelets and FFP accordingly
For acute blood loss anemia, contemporary protocols suggest a 1:1 or 1:2 replacement of PRBCs: FFP
In an emergency, anyone can receive type O PRBCs (preferably O negative), and type AB individuals can receive PRBCs of any ABO type. People with type O blood are “universal donors,” and those with type AB blood are “universal recipients.” In addition, AB plasma donors can give to all blood types
RISKS OF TRANSMISSION
Hepatitis C virus | 1:1.6 million |
Hepatitis B virus | 1:180 000 |
Human immunodeficiency virus | 1:1.9 million |
Fatal red cell hemolytic reaction | 1:250 000-1.1 million |
Delayed red cell hemolysis | 1:1 000–1 500 |
Transfusion-related acute lung injury (TRALI) | 1:5 000 |
Febrile red cell nonhemolytic reaction | 1:100 |
Allergic (urticarial reaction) | 1:100 |
Anaphylactic reaction | 1:150 000 |
Improves gas exchange and decreases the work of breathing
Classified by manner in which inspiration is terminated. Most common are
Volume—cycled
Pressure—cycled
Flow—cycled
Time—cycled
Majority of postsurgical patients will be on volume-cycled ventilation with pressure support
Inspiratory phase terminated after delivery of a preset tidal volume
Physician sets inspiratory flow, tidal volume, and respiratory rate
Airway pressure and inspiratory time are patient related
Three common modes of volume-cycled ventilation
CMV: Controlled Mechanical Ventilation
The minute ventilation is completely a function of the preset respiratory rate and tidal volume. Patient’s efforts do not contribute to ventilation. Suitable for a patient making no respiratory effort
A/C: Assist-Control
The ventilator responds to patient’s inspiratory effort by supplying a preset tidal volume. A control mode backup ensures against hypoventilation
IMV: Intermittent Mandatory Ventilation
A preset tidal volume and respiratory rate triggers automatically at timed intervals. Most of these mechanical breaths are synchronized with an inspiratory effort by the patient [synchronized intermittent mandatory ventilation (SIMV)]
Triggered by patient’s inspiration; tidal volume and respiratory rate are not set
Inspiration is terminated when a set flow rate is reached
Pressure support [eg, positive end expiratory pressure (PEEP)] is a flow-cycled ventilation
Preset pressure is sustained until the patient’s inspiratory flow tapers to a set percentage of its maximum value
Pressure support decreases the work of breathing; requires the patient to initiate their own breath
Useful in combination with SIMV when weaning a patient
Tidal volume: Approximately 8 mL/kg ideal body weight. Inversely proportional to Paco2. This does not apply to patients on an acute respiratory distress syndrome (ARDS) protocol. Paco2 is affected by minute ventilation and tidal volume
Respiratory Rate: Product of respiratory rate and tidal volume is minute ventilation. Usually between 12 and 16 per minute
Trigger mode: Ventilator senses negative airway pressure and responds with a “triggered” breath. Usual sensitivity is –1 to –3 cm H2O
PEEP: Improves V/Q matching and therefore gas exchange
Fio2: Always attempt to minimize while maintaining SaO2
Flow rate: Adjusted to provide appropriate I/E ratio, typically 1:3
Hypoxemic respiratory failure
Chest x-ray typically reveals bilateral alveolar infiltrates
Often accompanied with acute respiratory alkalosis and high A-a gradient
Pulmonary Capillary Wedge Pressure (PCWP) less than 18 is classic; however, not on updated criteria
Pao2/Fio2 less than 300
Attempt to keep plateau pressures less than 30 cm H2O
Keep tidal volumes low
Increase PEEP before Fio2
Refer to ARDSnet.org for protocol
Certain goals must be met prior to weaning patients off the ventilator
First and foremost, a patient’s level of alertness should be assessed prior to extubation—a patient should be alert enough to handle their own secretions and be able to mentate
Assessing how a patient will do on minimal ventilator settings for a period of time prior to extubation is important—Minimal ventilator settings at our institution are pressure support 5, PEEP 5, Fio2 40%
Assessing a patient’s volume status prior to extubation is equally important. Patients who have required liters of fluid for resuscitation may benefit from Lasix to diurese some of this fluid (and hence increase lung compliance) prior to extubation
Tobin/RSBI
RSBI: Rapid Shallow Breathing Index (ratio of respiratory frequency/tidal volume) of less than 105 breaths/L/min has been associated with weaning success. Patients breathing in large tidal volumes and not hyperventilating will likely have lower RSBIs and an increased chance of weaning off sedation
Ideally their respiratory rate is under 25 breaths/min
NIF: Negative Inspiratory Force more negative than −20 mm Hg is ideal. The NIF measures the strength of respiratory muscles. Tested by asking patients to suck up air through the ET tube
A positive cuff leak (air moving through the trachea when the cuff is deflated) indicates that laryngeal edema is most likely NOT present; thus, the airway will not be compromised if extubated
Vital Capacity: For weaning this should be 10–15 mL/kg of ideal body weight, tidal volume 2–3 mL/kg of ideal body weight
Sepsis: Anion gap metabolic acidosis
Renal Tubular Acidosis: Non-anion gap metabolic acidosis
Urinary diversion: Non-anion gap metabolic acidosis
Vomiting is least likely to produce acidosis
Prolonged NG tube use can lead to persistent metabolic alkalosis
Normal values
pH: 7.35–7.45
HCO3: 22–26
Paco2: 38–42
Patient Evaluation
Acidemic or Alkalemic?
Check pH: <7.38 is acidemic; >7.42 is alkalemic
Overriding problem respiratory or metabolic?
Check Paco2, HCO3 (Table 3-6)
If metabolic acidosis present, is there an anion gap? (Check albumin)
Anion Gap = Na − (HCO3 + Cl)
Gap: >12; non-gap: <12
See Table 3-7
In metabolic disturbances, is the respiratory system compensating?
In metabolic acidosis
Check expected Paco2: [1.5 × HCO3] + 8 ± 2
If Paco2 < predicted, there is a coexisting respiratory alkalosis
If Paco2 > predicted, there is a coexisting respiratory acidosis
In metabolic alkalosis
If Paco2 < 40, there is a coexisting primary respiratory alkalosis
If Paco2 > 50, there is a coexisting primary respiratory acidosis
If a gap metabolic acidosis, are there other metabolic disturbances present?
Check corrected HCO3: Measure HCO3 + (anion gap−12)
If >24 there is a coexisting primary metabolic alkalosis
If <24, there is a coexisting non-gap metabolic acidosis
METABOLIC ACIDOSIS: ANION GAP VERSUS NON-GAP
Anion Gap (accumulation of organic acid, H+) | Non-anion Gap (loss of HCO3) |
---|---|
(MUDPILES) Methanol/Metformin Uremia/Renal failure Diabetic ketoacidosis Paraldehyde Iron, isoniazid, inhalants, isopropyl alcohol Lactic acidosis, sepsis Ethylene glycol Salicylates, aspirin, solvents | (HEART CCU) Hypoaldosterone/Addison’s Disease Expansion with IV fluids Acid ingestion Renal tubular acidosis Turds (diarrhea) Chronic pyelonephritis Carbonic anhydrase inhibitors (acetazolamide) Urinary diversions, GI losses |
Treatment | |
Treat underlying cause | Give HCO3 (if PaCO2 is less than 20) |
Calculate Fractional Excretion of Sodium (FENa)
Determines if renal failure is due to prerenal, postrenal, or intrinsic renal pathology (Table 3-8)
FENa (%) = [(Urine Na × Plasma Cr/Plasma Na × Urine Cr) × 100]
Prerenal: FENa <1%: low volume, pump failure
Postrenal: Obstruction (cervical cancer, ureteral injury, etc)
Intrinsic: Tubular (granular casts, Urine Na >40, BUN/Cr <15; from ischemia, drugs, rhabdomyolysis); interstitial (white blood cells, eosinophils; from drugs, pyelonephritis); glomerular (RBCs, RBC casts, proteinuria; from post-strep, connective tissue diseases); vascular (vasculitis, DIC, malignant hypertension)
Remember: Renally dose Vancomycin. Obtain Vancomycin levels after the third dose and 1 hour prior to the fourth dose
HEMODYNAMIC PARAMETERS
Parameter | Normal Value |
---|---|
Systemic Vascular Resistance (SVR) | 800–1200 dynes/s/cm5 |
Cardiac Output (CO) | 4–8 L/min |
Mean Arterial Pressure (MAP) | 70–105 mm Hg |
Central Venous Pressure (CVP) or Right Atrial Pressure | 2–8 mm Hg |
Pulmonary Capillary Wedge Pressure (PCWP) | 5–12 mm Hg |
Pulmonary Artery Pressure (PAP) | 15–30 mm Hg |
TYPES OF SHOCK
Mechanism | Measurements | Management | Miscellaneous | |
---|---|---|---|---|
Septic shock | Vascular tone is lost in arteries and veins (increased vascular capacitance) | Low PCWP High CO Low SVR Low CVP Low PCWP | Antibiotics Volume Dopamine or norepinephrine No dobutamine | TNF-alpha Initiator = IL2 |
Hemorrhagic shock | Decreased volume, decreased ventricular filling | Low CO High SVR Low CVP | VOLUME! NaHCO3 if acidotic Avoid pressors | |
Cardiogenic shock | Decreased cardiac function (decreased CO) leads to venous congestion | High PCWP Low CO High SVR High CVP | Dobutamine | ECHO can help differentiate |
Most common gynecologic malignancy in the world
Second most frequently diagnosed cancer worldwide after breast cancer
Third most common gynecologic malignancy in the United States and third most common cause of gynecologic cancer death
0.68% lifetime risk of cervical cancer (1 in 147 women) in the United States
Half of women diagnosed are 35 to 55 years old
Mean age at diagnosis is 48 years; bimodal distribution with peaks at 35–39 and 60–64 years
Overall 5-year survival rate (SEER data 1999–2006): 70.2%. If localized, 91%
Incidence by Race: Hispanic > Black > White > American Indian > Asian/Pacific Islander
Infection: HPV 16, 18, 31, 33, 45, 51–53; HSV, chlamydia likely cofactors
HPV 16 accounts for 40–70% of invasive cervical cancers
HPV 18 is less prevalent but may be associated with cervical cancers that rapidly progress
First intercourse less than age 16 (first intercourse over age 20 reduces risk)
Multiple partners
Increased parity
Cigarette smoking
Immunosuppression (HIV, Fanconi anemia, chronic steroids, transplant)
Low socioeconomic status
Squamous cell carcinoma: Keratinizing, nonkeratinizing, verrucous, condylomatous, papillary, lymphoepithelioma-like
Adenocarcinoma: Mucinous (endocervical/intestinal/signet ring type), endometrioid (endometrioid AC with squamous metaplasia), clear cell, serous, minimal deviation (endocervical/endometrioid type), mesonephric, well-differentiated villoglandular
Other epithelial: Adenosquamous, glassy cell, mucoepidermoid, adenoid cystic, adenoid basal, carcinoid-like tumor, small cell, undifferentiated
Early: Asymptomatic
Late: Constitutional (anorexia, weight loss, weakness); vaginal bleeding (irregular, postcoital) serosanguineous or yellow discharge; pain (abdominopelvic, low back, dyspareunia); urinary frequency; lower extremity edema; hydronephrosis/acute renal failure; hemoptysis
Laboratory findings: Anemia, thrombocytosis, elevated creatinine
Screening: Pap and HPV testing [see current American Society for Colposcopy and Cervical Pathology (ASCCP) guidelines]
Diagnosis: Colposcopy with biopsy, endocervical curettage (ECC), excisional procedures (cold knife cone (CKC), loop electrosurgical excision procedure (LEEP))
Assessing disease status: Ultrasound, abdomen/pelvis CT, MRI, PET/CT
Cervical cancer spreads via
Direct invasion into cervical stroma, corpus, vagina, and parametrium
Lymphatic spread into cardinal ligament (causing ureteral obstruction), parametrial lymph vessels, lymph nodes of obturator, external iliac, and hypogastric vessels; parametrial, inferior gluteal, and presacral nodes; common iliac, para-aortic, inguinal, supraclavicular nodes (usually left)
Hematogenous
Intraperitoneal
FIGO standards
Permitted: Inspection, palpation, colposcopy, ECC, biopsies of cervix including conization, bladder, rectum, hysteroscopy, cystoscopy, proctoscopy, intravenous urography, and radiographic examination of the chest and skeleton
NOT included: Lymphangiograms, arteriograms, CT, MRI, PET, laparoscopy, laparotomy. (But, these may help plan treatment)
REVISED FIGO STAGING (2010) (Table 3-11)
Remains a clinically staged disease
Use of diagnostic imaging techniques to assess size of primary tumor is encouraged but is not mandatory. Imaging studies improve assessment/treatment of disease, but >80% of cervical cancer occurs where PET/CT/MRI are not readily available
Examination under anesthesia, cystoscopy, sigmoidoscopy, and IV pyelography is optional and no longer mandatory
Diagnostic excision technique recommended is CKC not LEEP
FIGO STAGING—CERVICAL CANCER
FIGO Staging—Cervical Cancer | |
---|---|
Stage I | Cancer confined to the cervix |
IA | Invasive cancer which can be diagnosed only by microscopy, with maximum depth ≤5 mm and horizontal spread ≤7mm |
IA1 | Measured stromal invasion of ≤3 mm in depth and horizontal spread ≤7 mm |
IA2 | Measured stromal invasion of >3 mm but not >5 mm with horizontal spread ≤7 mm |
IB* | Clinically visible lesions limited to cervix or preclinical cancers greater than stage IA2 |
IB1 | Clinically visible lesion ≤4 cm in greatest dimension |
IB2 | Clinically visible lesion >4 cm in greatest dimension |
Stage II | Cancer invades beyond uterus, but not to pelvic wall or lower third of vagina |
IIA | Without parametrial invasion |
IIA1 | Clinically visible lesion, extends to the upper third of the vagina, ≤4 cm in greatest dimension |
IIA2 | Clinically visible lesion, extends to the upper third of the vagina, >4 cm in greatest dimension |
IIB | With obvious parametrial invasion |
Stage III† | Cancer extends to pelvic wall and/or involves lower third of vagina and/or causes hydronephrosis or nonfunctioning kidney |
IIIA | Tumor involves the lower third of vagina, with no extension to pelvic wall |
IIIB | Extension to pelvic wall and/or hydronephrosis or nonfunctioning kidney |
Stage IV | Cancer extends beyond the true pelvis or involves (biopsy-proven) the mucosa of bladder or rectum (bullous edema does not permit allotment to Stage IV) |
IVA | Spread or growth to adjacent organs (including bladder or rectum) |
IVB | Spread to distant organs (liver, lung, distant lymph nodes) |
Primary surgical management is limited to stages I–IIA (Table 3-13)
Advantages to surgical treatment, particularly for younger women: Allows for thorough pelvic/abdominal exploration, individualized therapy plan, and ovarian conservation with transposition out of radiation field
Ovarian function conserved in fewer than 50% of patients with radiation
Fertility sparing techniques (Table 3-14)
Types of hysterectomies (Table 3-15) and differences among the types (Table 3-16) are shown in the tables
SURGICAL MANAGEMENT OF CERVICAL CANCER
Lymph Node (LN) and Recurrence Risk | Treatment | Miscellaneous | |
---|---|---|---|
Microinvasive Disease (IA1) | 0.5–1.2% LN Mets Recurrence: 1% | Simple Hyst (type I), CKC, or simple trachelectomy. Oophorectomy optional | |
Adenocarcinoma | 1.5% LN Mets Recurrence: 2.5% | ||
Stage IA2 | 5–7% LN Mets Recurrence: 3–5% | Can consider radical trachelectomy with lymphadenectomy and cerclage if fertility preservation is the goal | |
Stage IB1 | 13–15% LN Mets 5 year survival: 90% | In IB–IIA tumors, surgery and radiation are equivalent in terms of survival | |
Stage IB2 | 24–44% LN Mets 5 year survival: 70–73% | ||
Stages IB–IIA |