Fluid, Electrolyte and Acid-Base Balance

 Body fluid – Water and electrolyte

 Body water – Water alone
 Fluid Compartments:
o Cells
o Blood Vessels
o Tissue space (between blood vessels and cells)
 Factor affecting fluid and electrolyte balance
o Age
 The smaller the body; the larger the fluid
 In elderly, body water diminishes because of tissue loss can
reduce to 45-50% over 65yr
o Lifestyle (stress, exercise, warm or humid environment, and diet)
 Stress – Increased blood volume and decreased urine
production with increased ADH levels
 Fluid Distrubances:
o Fluid Volume Excess
 When patient have increased intravascular and interstitial
fluid retention and edema
 Peripheral – extremities or Pulmonary – lung tissue
 Factors:
 Excessive intake of fluid (IV therapy and sodium)
 Increased loss or decreased of protein intake
 Decreased IV movement
 Lymphatic organ obstruction
 Medication (steroid)
 Allergic
 Assessment findings :
 Acute weight gain
 Decreased BUN; Albumin; Hgb, Hct
 Increased central venous pressure


o Fluid Volume Deficit
 Intracellular; intravascular and interstitial dehydration
 Cause:
 Excessive fluid loss
  Diabetes insipidus
 Diabetes mellitus
 Addison’s diseases
 GI fistula or draining abscess
 Interstitial obstruction
 Assesment findings:
 Thirst
 Weight loss
 Mucous membrane and skin are dry
 Low grade temperature elevation
 Tachychardia
 Respiration increased
 Decrease urine output
 Concentrated urine
 Acid blood pH
 Severe : systolic BP decreased
 Electrolyte Disturbances
o Sodium:
 Primary determinant of Extracellular fluid (high
concentration and inability to cross the cell membrane
easily)
 Sodium can produce profound CNS effects on cognition and
sensory perception and on circulating blood volume
 Hyponatremia
 Cause :
o Increase water volume or Sodium deficit
o Hyposmolar state (ratio of water to sodium is
too high) water will move out to interstitial
space and intracellular space causing edema
 Hypernatremia
 Cause:
o Reverse from hyponatremia
o Hyperosmolar (Increase extracellular osmotic
pressure)
o Potassium:
 Normal range 3.5-5.0 mEq/l
 Reciprocal effect between sodium and potassium ( large
sodium intake result large potassium loss, vice versa)
 Two categories of diuretics:
 Potassium-wasting diuretics (furosemide)
o Excrete potassium and other electrolytes
(sodium and chloride)
 Potassium sparing diuretics ( Spirmolactine)
o Retain potassium but excrete sodium and
chloride
o Calcium:
 99% deposited in bone as phosphate and carbonate
 1% in blood plasma (serum)
  50% of Ca in serum will be ionized with remaining 50%
bound to protein
 Free ionized need for cell permeability; and Ca that bound
to protein can pass the capillary wall and stay in IV
compartment
 Ca absorption and utilization require adequate vit D and
protein
 Ca important for blood clotting mechanism; maintaining
neuromuscular system and driving muscle contraction
 Hypocalcemia:
 Alkalosis
 Elevated albumin

Hypercalcemia:
 Decrease neuromuscular activity


o Magnesium:
 Higher in cerebrospinal fluid
 Hypomagnesia:
 Neurologic, neuromuscular and cardiovascular
system
  Hypermagnesia:
 Clinical manifestation are nonspecific


o Phosphate

o
 o
o Chloride
 Chloride and water will move together will sodium
 Although chloride usually follow sodium, the proportion
will be different, because loss in chloride can be
compensated by increase of bicarbonate
 Hyperchloremia:
 Dehydration hypernatremia and metabolic acidosis
 Sign and symptoms:
o Muscle weakness, deep and rapid breathing,
lethargy
 Hypochloremia:
 Compensated by bicarbonate so cause metabolic
alkalosis
 Sign and symptoms: Muscle twitching and slow;
shallow breathing
 Assessment:
o Physical examination:
 Vital signs
 Increased pulse rate and lower BP in FVD
 Edema
 Can be localized or generalized
 Localized characterized :
o Taut
o Smooth
o Shinny
o Pale skin
 Inspect the dependent body: Sacrum, back and legs
 Skin turgor
  Pinched and released will back to the normal
position because the outward pressure on
extracellular and interstitial fluid
 Oral cavity
 Eyes
 FVD – Sunken eyes, dry conjunctiva, decrease or
absent tearing
 FVE – periorbital edema with history of blurred eyes
 Jugular and Hand veins
 Place the patient in fowler’s position

 Palpate the jugular veins

o FVE cause distention
 Place the client’s hand below the heart level, palpate
the jugular veins
o FVD decrease venous filling (flat neck veins)
 Neuromuscular system
 Measure the osmolality
 Measure of total concentration of dissolved particle
per kg of water
 Serum of urine
  Normal serum osmolality 280-295mOsm/kg
o Increased in FVD
o Decreased in FVE
 Osmolality concentration of solutes in total body of
water (solute per kg of body weight) rather than in
cellular fluid (osmolarity)
 IV therapy terms of osmolarity is more appropriate
o Hypotonic
o Isotonic
o Hypertonic
 Urine osmolality
o Solutes/particles measure in urine are
nitrogenous waste (creatinine, urea, uric
acid)
 Urine pH
 Will increase in FVD if the renal fail to respond the
pH in blood

DVT and Pulmonary Thromboembolism

 Survivor may succumb to disabilities of chronic thromboembolic

pulmonary hypertension and postthrombotic syndrome
 Chronic thromboembolic Pulmonary Ht causes breathlessness with
exertion
 Postthrombotic syndrome (chronic venous insufficiency) damages the
venous valves of the leg and cause ankle or calf swelling and leg aching,
can cause skin ulceration
 Pathophysiology:
o Inflammation and Platelet Activation
 Virchow’s triad of inflammation, hypercoagulability, and
endothelial injury leads to recruitment of activated
platelets, which release microparticles. These
microparticles contain proinflammatory mediators that
bind neutrophils, stimulating them to release their nuclear
material and form web-like extracellular networks called
neutrophil extracellular traps. These prothrombotic
networks contain histones that stimulate platelet
aggregation and promote platelet-dependent thrombin
generation. Venous thrombi form and flourish in an
environment of stasis, low oxygen tension, and
upregulation of proinflammatory genes.
o Protrombotic states
 The two most common autosomal dominant genetic
mutations are factor V Leiden, which causes resistance to
the endogenous anticoagulant, activated protein C (which
inactivates clotting factors V and VIII), and the prothrombin
gene mutation, which increases the plasma prothrombin
 concentration (Chaps. 78 and 142). Antithrombin, protein
C, and protein S are naturally occurring coagulation
inhibitors. Deficiencies of these inhibitors are associated
with VTE but are rare. Antiphospholipid antibody
syndrome is the most common acquired cause of
thrombophilia (increased thrombosit) and is associated
with venous or arterial thrombosis. Other common
predisposing factors include cancer, obesity, cigarette
smoking, systemic arterial hypertension, chronic
obstructive pulmonary disease, chronic kidney disease,
blood transfusion, long-haul air travel, air pollution, oral
contraceptives, pregnancy, postmenopausal hormone
replacement, surgery, and trauma.
o Embolization
 When deep venous thrombi (Fig. 300-2) detach from their
site of formation, they embolize to the vena cava, right
atrium, and right ventricle, and lodge in the pulmonary
arterial circulation, thereby causing acute PE. Paradoxically,
these thrombi occasionally embolize to the arterial
circulation through a patent foramen ovale or atrial septal
defect. Many patients with PE have no evidence of DVT
because the clot has already embolized to the lungs.
 Treatment
 TREATMENT Deep Venous Thrombosis PRIMARY THERAPY
 Primary therapy consists of clot dissolution with pharmacomechanical therapy that usually
includes low-dose catheter-directed thrombolysis. This approach is reserved for patients with
extensive femoral, iliofemoral, or upper extremity DVT. The open vein hypothesis postulates
that patients who receive primary therapy will sustain less long-term damage to venous
valves, with consequent lower rates of postthrombotic syndrome. A National Heart, Lung, and
Blood Institute–sponsored randomized controlled trial called ATTRACT (NCT00790335) is
testing this hypothesis.
 SECONDARY PREVENTION
 Anticoagulation or placement of an inferior vena caval filter constitutes secondary prevention
of VTE. To lessen the severity of postthrombotic syndrome of the legs, below-knee graduated
compression stockings may be prescribed, 30–40 mmHg, for 2 years after the DVT episode.
They should be replaced every 3 months because they lose their elasticity.
 TREATMENT Pulmonary Embolism RISK STRATIFICATION
 Hemodynamic instability, RV dysfunction on echocardiography, RV enlargement on chest
CT, or elevation of the troponin level due to RV microinfarction portend a high risk of an
adverse clinical outcome. When RV function remains normal in a hemodynamically stable
patient, a good clinical outcome is highly likely with anticoagulation alone (Fig. 300-7).
 ANTICOAGULATION
 Effective anticoagulation is the foundation for successful treatment of DVT and PE. There are
three options: (1) the conventional strategy of parenteral therapy “bridged” to warfarin, (2)
parenteral therapy “bridged” to a novel oral anticoagulant such as dabigatran (a direct
thrombin inhibitor) or edoxaban (an anti-Xa agent), or (3) oral anticoagulation with
rivaroxaban or apixaban (both are anti-Xa agents) with a loading dose followed by a
maintenance dose as monotherapy without parenteral anticoagulation.
 The three heparin-based parenteral anticoagulants are (1) unfractionated heparin (UFH), (2)
low-molecular-weight heparin (LMWH), and (3) fondaparinux. For patients with suspected or
proven heparin-induced thrombocytopenia, there are two parenteral direct thrombin inhibitors:
argatroban and bivalirudin (Table 300-3).
 Unfractionated Heparin
 UFH anticoagulates by binding to and accelerating the activity of antithrombin, thus
preventing additional thrombus formation. UFH is dosed to achieve a target activated partial
thromboplastin time (aPTT) of 60–80 s. The most popular nomogram uses an initial bolus of
80 U/kg, followed by an initial infusion rate of 18 U/kg per h.
 The major advantage of UFH is its short half-life, which is especially useful in patients in
whom hour-to-hour control of the intensity of anticoagulation is desired.
 Low-Molecular-Weight Heparins
 These fragments of UFH exhibit less binding to plasma proteins and endothelial cells and
consequently have greater bioavailability, a more predictable dose response, and a longer half-
life than does UFH. No monitoring or dose adjustment is needed unless the patient is
markedly obese or has chronic kidney disease.
 Fondaparinux
 Fondaparinux, an anti-Xa pentasaccharide, is administered as a weight-based once-daily
subcutaneous injection in a prefilled syringe. No laboratory monitoring is required.
Fondaparinux is synthesized in a laboratory and, unlike LMWH or UFH, is not derived from
animal products. It does not cause heparin-induced thrombocytopenia. The dose must be
adjusted downward for patients with renal dysfunction.
 Warfarin
 This vitamin K antagonist prevents carboxylation activation of coagulation factors II, VII, IX,
and X. The full effect of warfarin requires at least 5 days, even if the prothrombin time, used
for monitoring, becomes elevated more rapidly. If warfarin is initiated as monotherapy during
an acute thrombotic illness, a paradoxical exacerbation of hypercoagulability increases the
likelihood of thrombosis. Overlapping UFH, LMWH, fondaparinux, or parenteral direct
thrombin inhibitors with warfarin for at least 5 days will nullify the early procoagulant effect
of warfarin.
 WARFARIN DOSING
 In an average-size adult, warfarin is often initiated in a dose of 5 mg. The prothrombin time is
standardized by calculating the international normalized ratio (INR), which assesses the
anticoagulant effect of warfarin (Chap. 78). The target INR is usually 2.5, with a range of
2.0–3.0.
 The warfarin dose is usually titrated empirically to achieve the target INR. Proper dosing is
difficult because hundreds of drug-drug and drug-food interactions affect warfarin
metabolism. Increasing age and systemic illness reduce the required warfarin dose.
Pharmacogenomics may provide more precise initial dosing of warfarin. CYP2C9 variant
alleles impair the hydroxylation of S-warfarin, thereby lowering the dose requirement.
Variants in the gene encoding the vitamin K epoxide reductase complex 1 (VKORC1) can
predict whether patients require low, moderate, or high warfarin doses.
 Centralized anticoagulation clinics have improved the efficacy and safety of warfarin dosing.
Patients can self-monitor their INR with a home point-of-care fingerstick machine and can
occasionally be taught to self-dose their warfarin.
 Novel Oral Anticoagulants
 Novel oral anticoagulants are administered in a fixed dose, establish effective anticoagulation
within hours of ingestion, require no laboratory coagulation monitoring, and have few of the
drug-drug or drug-food interactions that make warfarin so difficult to dose. Rivaroxaban, a
factor Xa inhibitor, is approved for treatment of acute DVT and acute PE as monotherapy,
without a parenteral “bridging” anticoagulant. Apixaban is likely to receive similar approval
for oral monotherapy. Dabigatran, a direct thrombin inhibitor, and edoxaban, a factor Xa
inhibitor, are likely to be approved for treatment of VTE after an initial course of parenteral
anticoagulation.
 Complications of Anticoagulants
 The most serious adverse effect of anticoagulation is hemorrhage. For life-threatening or
intracranial hemorrhage due to heparin or LMWH, protamine sulfate can be administered.
Heparin-induced thrombocytopenia is less common with LMWH than with UFH. There is no
specific reversal agent for bleeding caused by fondaparinux, direct thrombin inhibitors, or
factor Xa inhibitors.
 Major bleeding from warfarin is best managed with prothrombin complex concentrate. With
serious but non–life-threatening bleeding, fresh-frozen plasma or intravenous vitamin K can
be used. Recombinant human coagulation factor VIIa (rFVIIa) is an off-label option to
manage catastrophic bleeding from warfarin, but prothrombin complex concentrate is a better
 choice. Oral vitamin K is effective for managing minor bleeding or an excessively high INR
in the absence of bleeding.
 Duration of Anticoagulation
 For DVT isolated to an upper extremity or calf that has been provoked by surgery, trauma,
estrogen, or an indwelling central venous catheter or pacemaker, 3 months of anticoagulation
usually suffice. For an initial episode of provoked proximal leg DVT or PE, 3 to 6 months of
anticoagulation are considered sufficient. For patients with cancer and VTE, prescribe LMWH
as monotherapy without warfarin and continue anticoagulation indefinitely unless the patient
is rendered cancer-free.
 Among patients with idiopathic, unprovoked VTE, the recurrence rate is high after cessation
of anticoagulation. VTE that occurs during long-haul air travel is considered unprovoked.
Unprovoked VTE may be caused by an exacerbation of an underlying inflammatory state and
can be conceptualized as a chronic illness, with latent periods between flares of recurrent
episodes. American College of Chest Physicians (ACCP) guidelines recommend considering
anticoagulation for an indefinite duration with a target INR between 2 and 3 for patients with
idiopathic VTE. An alternative approach after the first 6 months of anticoagulation is to
reduce the intensity of anticoagulation and to lower the target INR range to between 1.5 and 2.
 Counterintuitively, the presence of genetic mutations such as heterozygous factor V Leiden
and prothrombin gene mutation does not appear to increase the risk of recurrent VTE.
However, patients with antiphospholipid antibody syndrome may warrant indefinite-duration
anticoagulation, even if the initial VTE was provoked by trauma or surgery.
 INFERIOR VENA CAVAL (IVC) FILTERS
 The two principal indications for insertion of an IVC filter are (1) active bleeding that
precludes anticoagulation and (2) recurrent venous thrombosis despite intensive
anticoagulation. Prevention of recurrent PE in patients with right heart failure who are not
candidates for fibrinolysis and prophylaxis of extremely high-risk patients are “softer”
indications for filter placement. The filter itself may fail by permitting the passage of small-to
medium-size clots. Large thrombi may embolize to the pulmonary arteries via collateral veins
that develop. A more common complication is caval thrombosis with marked bilateral leg
swelling.
 Paradoxically, by providing a nidus for clot formation, filters increase the DVT rate, even
though they usually prevent PE (over the short term). Retrievable filters can now be placed for
patients with an anticipated temporary bleeding disorder or for patients at temporary high risk
of PE, such as individuals undergoing bariatric surgery who have a prior history of
perioperative PE. The filters can be retrieved up to several months after insertion unless
thrombus forms and is trapped within the filter. The retrievable filter becomes permanent if it
remains in place or if, for technical reasons such as rapid endothelialization, it cannot be
removed.
 MANAGEMENT OF MASSIVE PE
 For patients with massive PE and hypotension, replete volume with 500 mL of normal saline.
Additional fluid should be infused with extreme caution because excessive fluid
administration exacerbates RV wall stress, causes more profound RV ischemia, and worsens
LV compliance and filling by causing further interventricular septal shift toward the LV.
Dopamine and dobutamine are first-line inotropic agents for treatment of PE-related shock.
Maintain a low threshold for initiating these pressors. Often, a “trial-and-error” approach
works best; other agents that may be effective include norepinephrine, vasopressin, or
phenylephrine.
 FIBRINOLYSIS
 Successful fibrinolytic therapy rapidly reverses right heart failure and may result in a lower
rate of death and recurrent PE by (1) dissolving much of the anatomically obstructing
pulmonary arterial thrombus, (2) preventing the continued release of serotonin and other
neurohumoral factors that exacerbate pulmonary hypertension, and (3) lysing much of the
source of the thrombus in the pelvic or deep leg veins, thereby decreasing the likelihood of
recurrent PE.
 The preferred fibrinolytic regimen is 100 mg of recombinant tissue plasminogen activator
(tPA) administered as a continuous peripheral intravenous infusion over 2 h. The sooner
thrombolysis is administered, the more effective it is. However, this approach can be used for
at least 14 days after the PE has occurred.
 Contraindications to fibrinolysis include intracranial disease, recent surgery, and trauma. The
overall major bleeding rate is about 10%, including a 1–3% risk of intracranial hemorrhage.
Careful screening of patients for contraindications to fibrinolytic therapy (Chap. 295) is the
best way to minimize bleeding risk.
 The only Food and Drug Administration–approved indication for PE fibrinolysis is massive
PE. For patients with submassive PE, who have preserved systolic blood pressure but
moderate or severe RV dysfunction, use of fibrinolysis remains controversial. Results of a
1006-patient European multicentered randomized trial of submassive PE, using the
thrombolytic agent tenecteplase, were published in 2014. Death or hemodynamic collapse
within 7 days of randomization was reduced by 56% in the tenecteplase group. However,
hemorrhagic stroke occurred in 2% of tenecteplase patients versus 0.2% in patients who only
received heparin.
 PHARMACOMECHANICAL CATHETER-DIRECTED THERAPY
 Many patients have relative contraindications to full-dose thrombolysis. Pharmacomechanical
catheter-directed therapy usually combines physical fragmentation or pulverization of
thrombus with catheter-directed low-dose thrombolysis. Mechanical techniques include
catheter maceration and intentional embolization of clot more distally, suction thrombectomy,
rheolytic hydrolysis, and low-energy ultrasound-facilitated thrombolysis. The dose of
alteplase can be markedly reduced, usually to a range of 20 to 25 mg instead of the peripheral
intravenous systemic dose of 100 mg.
 PULMONARY EMBOLECTOMY
 The risk of major hemorrhage with systemically administered fibrinolysis has prompted a
renaissance of interest in surgical embolectomy, an operation that had almost become extinct.
More rapid referral before the onset of irreversible multisystem organ failure and improved
surgical technique have resulted in a high survival rate.
 PULMONARY THROMBOENDARTERECTOMY
 Chronic thromboembolic pulmonary hypertension develops in 2–4% of acute PE patients.
Therefore, PE patients who have initial pulmonary hypertension (usually diagnosed with
Doppler echocardiography) should be followed up at about 6 weeks with a repeat
echocardiogram to determine whether pulmonary arterial pressure has normalized. Patients
impaired by dyspnea due to chronic thromboembolic pulmonary hypertension should be
considered for pulmonary thromboendarterectomy, which, if successful, can markedly reduce,
and sometimes even cure, pulmonary hypertension (Chap. 304). The operation requires
median sternotomy, cardiopulmonary bypass, deep hypothermia, and periods of hypothermic
circulatory arrest. The mortality rate at experienced centers is approximately 5%. Inoperable
patients should be managed with pulmonary vasodilator therapy.
 EMOTIONAL SUPPORT
 Patients with VTE may feel overwhelmed when they learn that they are suffering from PE or
DVT. Some have never previously encountered serious cardiovascular illness. They wonder
whether they will be able to adapt to the new limitations imposed by anticoagulation. They
worry about the health of their families and the genetic implications of their illness. Those
who are advised to discontinue anticoagulation may feel especially vulnerable about the
potential for suffering recurrent VTE. At Brigham and Woman’s Hospital, a physician-nurse–
facilitated PE support group was initiated to address these concerns and has met monthly for
more than 20 years.

INTRAOPERATIVE MANAGEMENT
 Urinary catheter
o For the surgery that will take >4hrs
o Or the patient with history of urinary retention because of bladder
or prostate problem or patients taking or likely to be administered
potent diuretic
 NG tube
o Help empty stomach of gastric secretion, digested food, and
swallowed blood, thus lessening the likelihood of pulmonary
aspiration with gastric content regurgitation when patient is not in
total control of total upper airway
o Allow to decompress of stomach and reducing the possibility of the
postanesthesia nausea and vomiting
o Side effect, will produce some incompetence of gastroesophageal
sphincter, stimulate gastric secretion and are uncomfortable
 Hypotensive anaesthesia
o Consideration of the ischemia on the vulnerable organs (brain,
kidney, heart and liver) when blood flow is reduced below critical
levels
o Mean pressure around 50-60 mmHg considered safe for the brain
to maintain adequate flow
o Kidney

POSTOPERATIVE CONSIDERATIONS
Recovery from Anesthesia
 Most common problem is acute respiratory obstruction
 Factors involved:
o Soft tissue bleeding and edema due to surgery
o Tracheal and laryngeal edema due to trauma during intubation
o Ventilatory insufficiency due to pain after rib harvest and interjaw
fixation
 Pulse oxymetry has become the std for patient in recovery room
 Patient place in 30degree on the bed
 Suction setup should be available
 NG tube use to removed blood and other content of stomach that can
cause nausea
 Topical decongestants and humidified oxygen by mask helpful to
maintain nasal passage
Wound care
 Wound left alone in 24hr
 Oral hygiene procedure begin after 24 hr
Nutrition
 Usually will lose 4-8percent body weight in IMF, usually in first 2
postrugical weeks
 Weight lose more than 12-15lb should alert the surgeon to possible
problem with patient’s caloric intake
 Adult:
 o 30ml/kg/day
o Daily sodium and potassium 1mEq/kg/day
o Potassium needs during immediate postop period is usually
unnecessary in first 24hr, because the traumatized tissue will
provide potassium load released from injured cell
Fever
 Fever within first 24hr due to atelectasis or aspiration occurred during
surgery
 24-72hr, atelectasis (Complete or partial collapse of lung or lobe of lung,
develop in alveoli become deflated, common after GA because regular
patter change in breathing and absorption of gases and pressures) ,
pneumonia, and thrombophlebitis (vein inflammation related to
thrombus), which is secondary to IV catheter
 >72hr, pneumonia, PE, phlebitis, IV catheter sepsis, wound infection, UTI
(urinary tract infection)
 Most common in orthognatic surgery with usually health patient:
o Within 24hr – atelectasis
o 48-72hr – foley, IV line
o 72hr – 7 days – wound infection
 Others can be due to the blood transfusion and drugs used
Metabolic Disturbances
 If oral intake limited for 48hr, fluid and electrolyte abnormalities can
occur
 Third-space postoperative fluid collection very minimal in orthognatic
surgery, unless there is illium graft.
 Most common postop fluid disorder is volume overload by isotonic
expansion of extracellular fluid compartment. With characterized by:
o Increase BP
o Decrease Hb, hematocrit and serum protein level
 Water retention by ADH hormone also contribute to the volume
expansion
 Diuretic sometimes are necessary (low dose 10-25mg of furosemide)
Hemorrhage
 Postop bleeding can be due to the inadequate controlled bleeding during
intraoperative with hypotensive anesthesia, giving surgeon false
impression
 Most common side bleeding of the maxilla come from. Nasopalatine,
nasal-septal, and sphenopalatine arteries.
 Arterial embolization also another choice for postop bleeding, with
predictable risks include pain, trismus, transient cranial nerve palsies.
Unpredictable risks include skin necrosis, permanent cranial nerve
palsies, blindness, stroke and death.