Too Much Blood

by Jane Bennett Munro

  “I haven’t had sex with her,” he offered.

  “And I haven’t had sex with Bernie, either.”

  Hal put both palms on either side of my head and leaned on the door, looming over me. In the shadows, his face looked hooded and unreadable.

  Stubbornly, I stayed where I was. Hal leaned closer to me and looked deeply into my eyes. “I love you, Toni; you’re the only woman I will ever love. You’re the one I want to spend the rest of my life with and grow old with. You don’t need to worry about Bambi.”

  I slipped out from under his arms and stepped away, turning to look at him in disbelief. “Bambi? You’ve got to be kidding. Nobody is named Bambi, for God’s sake.”

  Hal straightened up and turned to face me. “That’s really her name, and she’s a very smart girl.”

  “Okay, so she’s smart. How smart is it to make a pass at a married professor?”

  “Okay. It’s not. She’s just a kid, and she’s lost her boyfriend. She’s emotionally overwrought. I can understand it.”

  Yeah, I could understand it too. Twenty years ago I had been the student who made a pass at a married professor and ended up marrying him. I should be able to forgive Bambi for doing the same thing. But was I willing to forgive Hal for responding to it? “You don’t have to encourage her, do you?”

  “I wasn’t encouraging her!”

  “How was taking her to lunch in an intimate booth in a dark bar not encouraging her?”

  “Toni …”

  “That’s two, Hal. Please don’t let there be a three.”

  Wednesday, December 17

  Chapter 16

  Marriage resembles a pair of shears,

  so joined that they cannot be separated;

  often moving in opposite directions,

  yet always punishing anyone who comes between them.

  —Sir Walter Scott

  All night I kept dreaming that the house was on fire and I couldn’t wake Hal. Then I’d wake up, and realize that there was no fire and that waking Hal was the last thing I wanted to do.

  I turned off the alarm before it rang and went to my aerobics class. Hal was still asleep when I got back, so I decided to let him sleep. I dressed in the bathroom and went to work, stopping in the cafeteria for coffee and danish.

  Since I was early, I went up to the nurses’ station and inquired about Tiffany and Lance. Tiffany had been released. Lance was in ICU.

  So I went down the hall to ICU, and on the way I met Jodi, accompanied by a nurse pushing Tiffany in a wheelchair. Tiffany looked pale, and her blonde hair was disheveled and stringy, but Jodi looked shell-shocked.

  “What’s the matter with you?” I demanded. “You look worse than she does.”

  “Thank you very much. Nice to see you too,” Jodi retorted. “Guess who else is in ICU.”

  Oh, no. “You don’t mean … Did Ruthie’s house burn down last night?”

  “No, no,” Jodi shook her head. “No, they’re all vomiting blood. Ruthie said it started last night with Angela having a nosebleed, and then Emily had one, and by morning everybody was sick.”

  “Is Ruthie sick too?” I wondered.

  “I don’t think so,” Jodi said. “She’s here with Lance.”

  “So how is Lance doing?” I asked. “Why is he in ICU?”

  “I don’t know,” Jodi said, “but he looks awful. You’ll see for yourself when you go in.”

  Jodi had not been exaggerating. Lance did look awful; he looked grayer and even more skeletal than before, if such a thing was possible—except for his swollen belly, which was visible under the covers and no doubt full of fluid. He had a central line in a subclavian vein through which a unit of blood was running, and a nasogastric tube with bloody drainage in it, attached to a Gomco pump on the floor. He was also unconscious, intubated, and on a respirator. His hands lay on the counterpane, jerking rhythmically. The whites of his half-open eyes appeared jaundiced.

  Ruthie sat by his bed, crying. “Oh, Toni, he’s so sick,” she sobbed. “He started throwing up blood yesterday, and then last night he couldn’t breathe, and they said he aspirated, and that’s when they put the tube down. They won’t tell me what’s wrong with him, and I’m afraid he’s going to die.”

  When I leaned over him to check his eyes, I was close enough to smell him, and it was like a flashback to medical school and my clinical rotations at the Long Beach Veteran’s Hospital.

  Upper GI bleeding. Ascites. Liver flap. Jaundice. Foetor hepaticus.

  Ruthie was worried with good reason. Lance was dying of liver failure.

  He was undoubtedly bleeding from esophageal varices—enlarged varicose veins in the esophagus caused by portal hypertension, which was increased blood pressure in the portal vein caused by cirrhosis of the liver. They can band those endoscopically these days, and I wondered why they hadn’t done it.

  Was Lance an alcoholic? That’s what it usually was, but I felt reluctant to ask Ruthie about such a potentially painful subject. So I changed the subject.

  “Looks like you’ve got your hands full here without having to deal with houseguests,” I said. “Do you need some help? They could come to our house when they leave here and save you a lot of work.”

  She dabbed her eyes, blew her nose, put the tissue in her purse and snapped it shut with a decisive gesture. “Thank you, but that won’t be necessary,” she assured me with a watery smile. “I enjoy their company. It takes my mind off things to have them around.”

  I patted her shoulder in what I hoped was a comforting gesture and went to the nurses’ station to check on the Burkes.

  Kathleen was in the cubicle next to Lance’s. I peeked in. She was asleep. She had an intravenous line in one hand and a nasogastric tube snaked from her nose to a Gomco pump similar to Lance’s. The contents were bloody. A bag containing bloody urine hung from the lower bedside rail. I stepped closer and checked what was going into her IV: fresh frozen plasma to replace her clotting factors.

  I stepped even closer and leaned over to smell her breath. It wasn’t minty fresh, but at least it wasn’t foetor hepaticus.

  Back in my office, I fired up the computer and looked at the electronic medical record, which turned up some very interesting findings.

  Kathleen’s lab work showed a partial thromboplastin time that was slightly elevated, and a prothrombin time and INR that were markedly elevated. Her platelet count and fibrinogen were normal. Perhaps the fresh frozen plasma she’d been receiving had corrected those already, but if so, it should have also corrected the PTT and pro-time. Had they also given her heparin? Or Coumadin? If so, maybe that explained things, but why would they do that?

  Not for the first time, I wished that the medical staff would get a clue and give up using the PTT to monitor heparin. It wasn’t because I hadn’t tried to educate them. There were so many factors that affected PTT besides heparin, and the anti-Xa—a measurement of activated clotting factor ten—was not affected by them and actually correlated with the amount of heparin in the blood. We had offered the test for the last year, and it was very rarely used, but I hadn’t yet given up on it.

  The pro-time and INR just didn’t make sense.

  Upstairs in Pediatric ICU, the children were being treated in a similar fashion and had similar lab results.

  Toxicology studies had been ordered on urine, and cultures on stool and blood, to rule out food poisoning, drug overdose, and enteric infections. But as far as I knew, none of these caused bleeding, with the exception of Campylobacter, which typically caused bloody diarrhea but not hematemesis—vomiting blood—or nosebleeds.

  Unless they’d all received an overdose of heparin.

  Oh, come on, Toni, get serious.

  Where would an entire family get an overdose of heparin? In the hospital? All of them? And in any case, weren’t t
hey all bleeding before they went to the hospital while they were still at Ruthie’s house?

  I was obviously hallucinating. So, to take my mind off it, I looked up Lance—and that’s where things really got weird.

  Like his late partner, Lance also had a history of deep vein thrombosis dating back to his early twenties; but instead of affecting the leg veins, as it did in most people, it had affected the portal, hepatic, and mesenteric veins, resulting in a series of hospitalizations for acute abdominal pain due to bowel and liver infarctions. He’d had an appendectomy and several small bowel resections.

  Our curmudgeonly gastroenterologist—George Marshall, he of the Gnarly Finger—had been his primary physician for at least twenty years, along with frequent consultations from the University of Utah, where some of Lance’s surgeries had been done.

  He’d been thoroughly worked up there for his coagulation problems and had been found to have the prothrombin mutation G20210A, a hereditary alteration in prothrombin, one of the major blood coagulation factors, which made him a very high risk for blood clots, and also resistant to Coumadin. So Lance was obliged to inject himself daily with enoxaparin, a low molecular weight heparin that was sold under the brand name Lovenox and could be given subcutaneously.

  No wonder he looked so dour. If I had to shoot up every day, I’d be right pissy too.

  According to the chart, nobody really knew why Lance had liver failure. He wasn’t an alcoholic. In fact, he rarely touched the stuff because of his history of liver infarctions; he didn’t want to cause any more damage. They attributed the bleeding to portal hypertension which is usually due to cirrhosis of the liver from chronic alcoholism, but in Lance’s case was probably due to scarring from multiple infarctions. The possibility of another hepatic or portal vein thrombosis, or possibly a liver tumor, was entertained.

  Usually a cirrhotic liver, or one with scarring from infarctions, was smaller than normal. But Lance’s was enlarged, with multiple nodules, which made tumor a distinct possibility. But was it a primary liver tumor—hepatocellular carcinoma—or metastatic tumor from some other source, such as colon, stomach, or pancreas? Or even lung? I doubted that; Lance wasn’t a smoker, as far as I knew. And how far had it spread? If they drew off some of that ascites fluid from his belly, would it have malignant cells in it?

  George was planning to get an MRI as soon as Lance was stable enough—and possibly a needle biopsy under CT guidance to get a diagnosis—and then start treatment. He said nothing about paracentesis or aspiration of all that ascitic fluid. I wondered why. Surely all of Lance’s abdominal organs were being compressed by it, not to mention his lungs from the diaphragm being pushed up into his chest. He also didn’t mention banding of esophageal varices. Maybe he didn’t think Lance was stable enough for that either, or maybe he was hoping Lance would throw a clot and plug them all up; but patients never throw clots where you want them to. They’re just ornery that way.

  George’s plan for an MRI and CT-guided needle biopsy was a worthy goal, I thought, and maybe he planned to remove fluid at the same time, but judging from what I was seeing, Lance would never stabilize and most likely would not survive long enough for any diagnostic procedure. In fact, I saw an autopsy in my future.

  I mentioned it to Mike. He gave me an eye-roll. “Oh, goody, a lawyer,” he groused. “I sure hope he dies soon enough that we can do the autopsy together. Sounds like it’s gonna be a bitch, I tell you what. Damn lawyer’s wife’ll probably sue just ’cause she is a damn lawyer’s wife.”

  I pretended to agree, but I was hoping Lance would hang on until the weekend when Mike was on call and I was on vacation. Still, I’d probably help Mike anyway, just out of curiosity. And let’s face it, Ruthie probably would sue.

  Wrongful death. Failure to diagnose. Failure to treat. The possibilities were endless. Here’s your list. Check all boxes that apply. Oh, and don’t forget loss of consortium, that’s always good for punitive damages.

  Mike was on call today, actually, and wouldn’t you know, he didn’t get a single goddamn frozen section all day. I, on the other hand, retired to my office, where I spent the next four hours reading out all of yesterday’s goddamn cases with all their goddamn frozen sections. Then I spent another hour proofreading them, editing them on the computer, and signing them out. And then I figured I’d better finish up Jay’s autopsy before I got any more calls about it.

  Besides, maybe it would get Bernie Kincaid out of Rollie’s hair, and that would be a good thing, whereas ongoing gossip and speculation would not. Be a good thing, I mean. No matter what Rollie promised me, such things do get around, and this is a small town, after all.

  I shuddered to think what would happen if Ruthie Brooks ever got wind of it. It would get around so fast, it’d stir up dust.

  After an autopsy, a lot more work remains to be done before it is actually completed and a final report prepared. Most people don’t realize that; they think that everything is obvious once the body is cut open, like on TV. Not so. That’s just the preliminary or provisional gross diagnosis, which is what I’d sent the police already. Samples of the tissues removed have to be processed and slides made and examined. In that respect, an autopsy is like a great big surgical case with many parts and subparts. It takes several days at best, and several months at worst.

  Unlike a medical examiner’s office, our practice predominantly involves surgical specimens on live patients, and their cases get done first.

  Then the lab work done on the postmortem blood samples has to be correlated with the autopsy findings. One has to hope they ordered the right tests in the first place to avoid the delay of having to order any more of them—assuming that the specimens are still any good—because you sure as hell can’t go back and get more.

  Finally, the autopsy findings from the tissue and the blood tests have to be correlated with the clinical picture; in other words, all the clinical findings should be explained by the autopsy findings.

  All that takes a lot longer than the gross autopsy examination does.

  Jay’s autopsy slides were not particularly illuminating. He had severe atherosclerosis in his coronary arteries, but none of them were blocked. There was slight patchy scarring in his heart, but nothing that looked like he’d had a heart attack—at least not forty-eight or more hours prior to death.

  His lungs were hemorrhagic, and there was aspiration pneumonia present, manifested by acute inflammation associated with food particles in the alveolar spaces of the lungs. His liver and spleen and all the sections of his gastrointestinal tract showed generalized congestion and interstitial hemorrhage, explaining the origin of all the bleeding thereof.

  None of this was unexpected.

  His lab tests were much more interesting than his slides.

  First, the carboxyhemoglobin was sixty-three percent, anything over fifty percent being lethal. That was the immediate cause of death.

  However, his bleeding problems were a contributing cause of death, particularly the brain hemorrhage. In the absence of carbon monoxide poisoning, respiratory failure and/or blood loss would have killed him. The cause of bleeding, however, was another question. What could have caused it?

  Once I knew that Jay’s postmortem prothrombin time and INR were not that far outside the therapeutic range, I was pretty sure that he didn’t die of an overdose of Coumadin. So what made him bleed to death? What else was there?

  Rat poison came to mind. Many years ago, rat poison contained arsenic or strychnine, but now many of them contain anticoagulants that are derivatives of warfarin, the origin of the drug Coumadin. In fact, some of them are super-warfarins that are resistant to Vitamin K, the antidote for Coumadin overdose. But this would also cause the prothrombin time and INR to be way out of the therapeutic range, so that was unlikely.

  Then there was heparin, which was used for acute treatment of patients newly diagnosed with
deep vein thrombosis or pulmonary embolus before they were switched to Coumadin. But Jay hadn’t been in the hospital, and heparin pretty much required hospitalization because it had to be given intravenously. It couldn’t be given orally because it was too large a molecule to be absorbed through the GI tract, and it couldn’t be given intramuscularly because it would cause hematomas or large painful hemorrhages in the muscle. Lovenox, a much smaller molecule, was given subcutaneously.

  Lance Brooks couldn’t take Coumadin, so he was using Lovenox at home. He could actually inject himself, or Ruthie could do it. Unlike regular heparin, it didn’t need to be monitored because it had a longer half-life, so it didn’t require hospitalization.

  Nothing is perfect, however. Cases of fatal or near-fatal hemorrhage with Lovenox were occasionally reported, and I had actually autopsied a couple of them in the last few years.

  So, although Lovenox didn’t need to be monitored, it could be, using the anti-Xa. And when I found out that Jay had not overdosed on Coumadin, I’d ordered one.

  It was markedly elevated.

  Someone had shot Jay Braithwaite Brooks full of heparin. Or Lovenox.

  But how? I wondered. Would Jay just sit there and allow someone to shoot him full of some unknown substance without at least asking a question or two? Wouldn’t he have resisted? Did the murderer have to hit him over the head and knock him out first? Was that the explanation for the subarachnoid hemorrhage and the contrecoup hemorrhage?

  So, assuming that to be the case, how was it possible for the murderer to hit Jay over the head hard enough to cause an intracerebral bleed without leaving a great big honking bruise on his scalp?

  And where were the injection marks? Although Jay had had purpura, there were no discrete hemorrhagic lesions such as what would have been present had he received multiple injections of an anticoagulant drug.

  So many questions; so few answers. But one question, I reflected, had an answer that was crystal clear.