resenta complicati ontogeni septic shot

Report of a case

Peter Quinn, D.M.D., M.D.,* and Louis H. Guernsey, D.D.S., M.S.D.,“” Philadelphia, Pa.

UNIVERSITY OF PENNSYLVANIA SCHOOL OF DENTAL MEDICINE AND HOSPITAL OF THE UNiVERSiTY OF PENNSYLVANIA

Although most odontogenic infections spread locally to adjacent fascial spaces, usually contiguous with the offending odontogenic pathosis, occasionally such an infection can spread rapidly across the midline and appear on the opposite side of the face and neck. Debilitated chronic alcohol abusers who are nutritionally deficient are more likely to develop serious life-threatening infections, either through serious airway involvement as seen in Ludwig’s angina or manifest as a gram-negative septicemia with life-threatening shock and even cardiac arrest, than the usual dental patient with cellulitis. Early recognition through a high index of suspicion and vigorous monitoring will pick up the initial manifestation of toxic shock. as noted in this case report. (ORAL SURG. ORAL MED. ORAL PATHOL. 5%336-339, 1985)

E arly recognition and treatment of shock is of utmost importance in reducing associated morbidity and mortality. It therefore behooves the clinician to appreciate the variability in clinical presentations of the patient in shock. Nowhere is this more evident than in the patient with sepsis. “Although the diag- nosis of shock is classically based on the presence of hypotension, poor tissue perfusion, oliguria, and metabolic acidosis, two or more of these are fre- quently absent in the patient with early septic shock.“’ Moreover, early in septic shock, a confusing clinical picture of increased cardiac output, increased pulse rate, and peripheral vasodilation may predominate. Most probably this “warm shock” syndrome is secondary to release of endotoxin.2 “‘Because of the potency of the endotoxin, there is rapid progression from ischemia to stagnant micro- circulation; the deterioration of the micro-circula- tion, which takes hours to occur in traumatic or hem’orrhagic shock, can occur in seconds or minutes following exposure to endotoxin.“3

*Assistant Professor of Oral and Maxillofacial Surgery, Director of the Oral and Maxillofacial Surgery Clinic, School of Dental Medicine; attending in Oral and Maxillofacial Surgery, Hospital of the University of Pennsylvania. **Professor and Chief of Oral and Maxillofaciai Surgery, Hospi- tal of the University of Pennsylvania; formerly Chairman, Oral and Maxillofacial Surgery Department, University of Pennsylva- nia School of Dental Medicine.

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It is this precipitous onset of symptoms which makes septic shock and its attendant complications so difficult to treat. Although immediate supportive therapy must be undertaken, it is vitally important to remember that the “treatment of septic shock has two separate objectives. The Jim is to control the initiating infectious process, primarily with antibiot- ics. The second objective is normalization of the patient’s hemodynamic state.“4

The purpose of this article is to report a case of septic shock secondary to odontogenic infection, which exhibits both the sudden onset and the severity of symptoms that can accompany this disease pro- cess.

CASEREPORT

On June 7, 1977, at approximately 620 P.M., a 6% year-old black man was referred to tlie emergency room of the Hospital of the University of Pennsylvania. One week prior to admission he had undergone a periodontal surgicai procedure on the right posterior mandibular quadrant. Three days prior to admission the patient began to experi- ence increasing swelling of the left side of the face and neck, difficulty in eating, and inability to open his mouth. He also reported intermittent episodes of fever and chills. On initial examination, he had a marked left facial and lateral neck cellulitis involving the left buccai, masticator, and submandibular spaces. He had moderate trismus, but intraoral examination was possible and revealed a partially edentulous maxilla and mandible with a periodontal pack-

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ing in the right posterior mandibular quadrant. There was no elevation of the tongue or any evidence of an acute intraoral infectious process. The patient was in mild respiratory distress, and auscultation revealed coarse inspi- ratory and expiratory rales throughout both lung fields. Pupils were equally round and reactive to light and accommodation. The fundi were benign, and the sclera were muddy. The patient was slightly disoriente,d. Initial vital signs were as follows: temperature, 103.2” F rectally; blood pressure, 150/90; pulse, 106 and regular; and respirations, shallow at a rate of 32 per minute. Significant laboratory values were as follows: hemoglobin, 10.8 gm; hematocrit, 35%; white blood cells, 8,800; urine, positive for protein, positive for red blood cells; glucose, 205 mg/dl; sodium, 145 mEq/L; potassium, 4.6 mEq/L; chloride, 98 mEq/L; bicarbonate, 22 mEq/L, blood urea nitrogen, 55 mg/dl; amylase, 825 U/L:

Aerobic and anaerobic blood specimens for culture were drawn, and the patient was started on 4 million units of aqueous penicillin every 4 hours and 600 mg of clindamy- tin every 8 hours. With the patient under local anesthesia, an incision and drainage procedure was performed from a 2 cm midline submental incision; Penrose drains were placed in the submental, right and left masticator spaces, and the left lateral neck (Fig. 1). Twenty-live cubic centimeters of fou’l-smelling suppurative drainage was obtained, and both aerobic and anaerobic ;specimens were sent for culture and sensitivity. Initial Gram stain showed numerous gram-positive rods, gram-negative rods, and gram-positive cocci, mostly single, with solme diplo- cocci. Following the incision and drainage, the patient was admitted to the floor. He was now oriented, and his vital signs were: stable with a rectal temperature of 100.8” F.

At 6 A.M. on June 8 the patient had an acute hypotensive episode. The blood pressure was 84/60 when th.e resident responded to the call. The hypotension responded quickly to Trendelenberg’s position and infusion of 1 liter of 5% dextrose in half-normal saline solution. At approximately 1 P.M. on the same day the patient again complained of dizziness and of not feeling at all well, with a rapid drop in pressure, while returning from the bathroom with a nurse in attendance. He collapsed and his vital signs deteriorated rapidly as he went into cardiorespiratory arrest. The patient was coded. Initially the e1ectrocardiogra.m showed asystole which responded to intravenous epinephrine and calcium chloride. The rate returned first to an idioventric- ular rhythm and then to normal sinus rhythm. Arterial blood gases showed severe metabolic acidosis with a pH of 6.981. The patient was intubated and transferred to the medical intensive care unit (MICU).

On admission to the MICU, the patient was given 7 ampules of bicarbonate and 1 ampule of calcium gluco- nate. A Swan-Ganz catheter was placed via the right femoral vein, and the initial pulmonary capillary wedge pressure was 18 cm of H,O. A radial arterial line gave an initial systolic reading of 85 to 95 but this fell to 50 systolic and the patient had to be maintained with a constant dopamine drip. The: patient was digitalized and placed on a

Fig. 1. Patient L.C., 65 years old, as he appeared on admission following incision and drainage under local anesthesia in the outpatient oral and maxillofacial surgery department.

Fig. 2. Patient as he appeared in the medical intensive care unit following cardiac arrest and oral intubation. Note that additional through-and-through Penrose drains have been placed to drain the infection further.

respirator with 100% 0, (Fig. 2). Blood specimens were again drawn and a Foley catheter was inserted.

The patient was completely anuric, despite an adequate wedge pressure, and was unresponsive to intravenous Lasix. A chest film showed consolidation of the right lower lobe, probably secondary to aspiration of exudate during

338 Quinn and Guernsey Oral Surg. April, 1985

The blood urea nitrogen and creatinine levels continued to increase, reaching values of 212 ( (creatinine) on June 12. Concomitantly, the urine output began to increase to 50 to LOO cc per hour, indicating the diuretic phase of acute tubular necrosis. Because of the uremia and a low calcium level, the renal consultant recommended dialysis. The metabolic balance was mark- edly improved within the first 24 hours of peritoneal dialysis.

Initial cultures of the wound were growing Bacteroides fragilis, Peptostreptococcus, Peptococcus, Bacteroides melaninogenicus, and Fusobacterium anaerobically. Aero- bically, Staphylococcus epidermis was growing but was considered to be a contaminant.

The patient’s upper gastrointestinal bleeding was sec- ondary to a stress ulcer, and a total of 8 units of blood was transfused over a 4-day period as his hemoglobin level had dropped to a low of 7.0 gm. The resultant anemia was aggravated by a chronic marrow depression confirmed by marrow aspirate that was thought to be secondary to ethanol abuse. An ora: tracheal tube was in place for a total of I3 days for immediate resuscitation and treatment of a bilateral gram-negative pneumonia. Gentamycin was added for this purpose.

Although there had been slow improvement in the cardiorespiratory, renal, and hematologic problems, the patient’s infection was spreading inferiorly along the cervical fascial planes. He developed a massive subcutane- ous, suprasternal Auctuance which, when drained, pro- duced 80 cc of thick greenish suppuration (Fig. 3). Penrose drains were placed, and communication with the neck incisions was evident with irrigation. Intraoral examina- tion now revealed 2+ to 3-t mobility of the five right posterior mandibular teeth, with suppuration drainage from the interdental areas. A lingual sequestrum second- ary to the original periodontal procedure was also present.

On July 8, 1977, with the patient under intravenous sedation and local anesthesia, the five teeth were removed. A small lesion at the apex of the first premolar had eroded through the inferior border of the mandible without radiographic evidence (Fig. 4).

The patient tolerated the procedure well, and over the next several days the cervical and suprasternal drainage completely ceased. He was afebrile and his mental status was markedly improved (Fig. 5). His pulmonary status continued to improve with daily chest physiotherapy and intermittent positive pressure breathing. Repeat electro- cardiograms had failed to show any significant myocardial damage secondary to the cardiac arrest, and renal function had returned to normal after vigorous dialysis. A complete return to oral feeding was delayed by a decreased gag reflex secondary to the prolonged intubation, and naso- gastric tube feedings were necessary for a short time.

On July 26 the patient was discharged (Fig. 6). His weight was 157.5 pounds, compared to an admission weight of 191 pounds. Vital signs were temperature, 98.6”F rectally; blood pressure, 130/70; respiration, 22 per

Fig. 3. Patient with nasogastric tube in place. This was productive of heme-positive coffee-ground aspirate from an acute upper gastrointestinal bleeding secondary to a stress ulcer.

Fig. 4. Patient now off the respirator and extubated. Yet his infection has continued to travel subcutaneously to the chest wall, producing a purulent exudate requiring further incision and drainage.

the arrest. A nasogastric tube was placed and a large amount of heme-positive, coffee-ground aspirate was obtained secondary to gastrointestinal upper bleeding (Fig. 3). At this point the patient was totally unresponsive, even to noxious stimuli.

The oliguria continued despite vigorous attempts at diuresis with Zaroxolyn, Mannitol, and Lasix, with an output of only 10 cc an hour. On June 9 the patient’s temperature spiked to 105” F, with continuing drainage of thick green pus from the lateral neck incision. By June 10 the patient’s blood pressure could be maintained in the range of llO-128/50-60 without the dopamine. His tem- perature was 100.2” F, and he was responding to simple commands. Blood cultures were negative.

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Fig. 5. Sites of extraction of five teeth which were in the primary periodontal surgery site and which, when removed, were found to be abscessed and the. primary cause of the lifc-threatening infection.

minute; pulse, 90 and regular. His hemoglobin level was 7.5 gm, but he was asymptomatic except for a slight tachycardia. The Hematology Service thought that he had an anemia of chronic disease and that transfusion was not necessary. Anemia of chronic disease is a mild to moderate (hematocrit usually 28% to 34%) under production anemia seen in a variety of chronic infectious, inflammatory, and malignant conditions.

SUMMARY AND DISCUSSION

We have presented a case of septic shock of odontogenic origin. We have attempted to summa- rize a 7-week hospitalization to illustrate the devas- tating complications of this syndrome, which in this case included cardiac arrest, acute renal failure, acute gastrointestinal bleeding, and aspiration pneu- monia.

Any serious infectious process of the head and neck must be suspect, especially in a susceptible patient, such as the one presented here. “Underlying host factors not alnly influence susceptibility of the patient to infection but also determine the likelihood of survival.“5 One of the major factors predisposing to septic shock is granulocytopenia, and paucity of healthy and vigorous polymorphonuclear leukocytes. This is very often Ipresent in ethanol-induced marrow depression. Studies have also suggested that a cir- rhotic liver is les;s able to clear bacteria from the blood.6

Fig. 6. Patient L.C. as he appeared on discharge from the hospital 49 days after gram-negative septic shock and cardiac arrest from an odontogenic infection.

Therefore, a thorough preoperative evaluation of any surgical patient, especially a compromised host, and a high index of suspicion in any postoperative infection are recommended so that one may react quickly to the septic shock syndrome should it develop.

REFERENCES

1. Wilson RF: The diagnosis and management of severe sepsis and septic shock. Heart and Lung 3: 422-429, 1976.

2. Donoff RB, Guralnick W: Shock due to odontogenic infec- tion: report of a case. J Oral Surg 35: 569-572, 1977.

3. Dietzman RH, Bloch JH, Lillehei RC: Treatment of shock. GP 36: 135-141, 1967.

4. Forgacs P: Treatment of septic shock. Med Clin North Am 63: 465-471, 1979.

5. Beeson PB: Cecil’s textbook of medicine, ed. 15, Philadelphia, 1979, W.B. Saunders Company, p. 1049.

6. Keusch GT, Weinstein L: Septic shock, Kalamazoo, 1977, The Upjohn Company, p. 6.

7. Reller LB, Sahn SA, Schrier RW: Clinical internal medicine, Boston, 1979, Little, Brown & Company, p. 253.

Reprint requests to: Dr. Louis H. Guernsey Department of Oral and Maxillofacial Surgery Hospital of the University of Pennsylvania 3400 Spruce St. Philadelphia, PA 19104